Vol. 69, No. 4 April 1952
ARCHIVES
PEDIATRICS
A MONTHLY DEVOTED TO THE
DISEASES OF INFANTS AND CHILDREN
JOHN FITCH LANDON, M.D., Editor
LEADING ARTICLES IN THIS NUMBER
Ascorbic Acid as a Chemotherapeutic Agent.
W.J. MeCormich,M.D. 151
The Cardiac Transition of the Newborn. Congenital Cardiac
Dilatation with Heart Block. Part II.
John A. Freel, M.D. 156
The Poison Cause of Poliomyelitis and Obstructions to Its
Investigation.
Ralph R. Scobey, MD. 172
E. B, TREAT & CO., Inc., Publishers, 45 East 17th Street, NEW YORK, 3
Yearly Subscription $6.00 (Foreign $€.75); Single Copy, $1.00
COPY RIGHT, 1952, BY EB. B. TREAT & CO., INC., ALL RIGHTS RESERVED
Entered as second-class matter Feb. 5, 1892, at New York, N. ¥., P. O., ander the Act of March 3, 1879
:
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triple sulfonamide therapy
Lice giving away candy . . . that’s how easy it is to
administer Truozine Dulcet Tablets to young patients
sulfonamide therapy is indicated.
These pale-green, sugary cubes are candylike in
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tability. Each cube contains 0,1 Gm. each of
Ifadiazine, sulfamerazine and sulfamethazine.
Dosage is accurate and dependable.
dministration is simple: Mother merely counts
wt the number of Truozive Dulcet Tablets you
escribe. They're supplied in bottles of 100 tablets.
Also available: Trvozine Suspension with
ium Citrate, each teaspoonful (5 ce.) containing
1 Gm. each of the three drugs, plus 1.5 Gm. of
dium citrate in a mint-flavored
ueous suspension. Bottles of 1 pint. Obbott
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Vitamins and minerals from
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rated in Pablum Mixed Ce-
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Recent improvements in
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You may prescribe Pablum
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PABLUM
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THE TRUTH ABOUT
FROZEN ORANGE JUICE
Significant Dietary Advantages Of
Fresh-Frozen Minute Maid Orange Juice
Over Home-Squeezed Orange Juice
Shown By Independent Research
ECENT assays ' emphasize the nutritional
superiority of reconstituted Minute Maid
Fresh-Frozen Orange Juice over home-squeezed
orange juice in three important respects:
@. Average levels of natural ascor-
bic acid were significantly higher
in Minute Maid;
b. Peel oil content was significantly
lower in Minute Maid;
¢. Bacterial counts were dramati-
cally lower in Minute Maid.
Two chief reasons for Minute Maid’s higher
ascorbic acid content are advanced by quali-
fied technical experts:
First, oranges vary widely in ascorbic acid
content due to differences in varieties, root-
stocks, and exposure to sunshine during ripen-
ing.” Thus, whole oranges, squeezed a few at a
time in the home, provide a highly erratic source
of Vitamin C. Yet because this vitamin is not
well-stored in the body, optimum nutrition
makes desirable a uniformly high intake. Each
can of Minute Maid, however, represents the
pooling of juice from hundreds of thousands of
oranges; thus wide variations in nutrients
from orange to orange tend to be eliminated.
Second, because it is frozen, Minute Maid
loses none of its ascorbic acid content during
the time lag between producer and consumer."
Whole fruit, however, is subjected to varia-
tions in temperature, and care in handling
cannot be maintained throughout the journey
from tree to table. Controlled laboratory tests
have shown an average ascorbic acid loss of
10.7% in whole oranges after 11 days under
simulated storage and shipping conditions.
Peel oil, previously shown to cause allergic
response and poor tolerance, especially in in-
fants,* is held to an arbitrary minimum in
Minute Maid. Samples of home-squeezed juice
expressed by typical housewives showed peel
oil contents up to 700% higher than Minute
Maid.
Bacterial counts were found to be as high as
350,000 per ml. in home-squeezed samples
but were uniformly low in Minute Maid. Tech-
nicians ascribe this to the combination of rigid
sanitary controls in the Minute Maid process
and the low pH and low temperatures at which
the juice is kept. In the case of home-squeezed
juice, high bacterial counts are doubtless due
to contamination from the exterior pee! which
is unknowingly added to the juice during
preparation.
In view of the above findings, more and more
physicians now specify Minute Maid Fresh-
Frozen Orange Juice in lieu of home-squeezed
orange juice where optimum year-around in-
take of natural Vitamin C is indicated.
REFERENCES
(1) Rakieten, M. L., et al.,
Journal of the American Dietet-
ic Association, October, 1951.
(2) U. S. Department of Agri-
culture Technical Bulletin No.
753, December, 1940.
(3) Roy, W. R., and Russell, H.
E., Food Industries, Vol. 20,
pp. 1764-1765 (1948).
(4) Joslin, C. L., and Bradley,
J. E., Journal of Pediatrics,
Vol. 39, No. 8, pp. 325-329
(1951).
MAID
Onanct
Juice
Reprints of Reference Material Mailed on Request
MINUTE MAID CORPORATION, 488 Madison Ave., New York 22, N.
Wallace R. Roy, Ph.D., Director of Research
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TO CONTRIBUTORS AND CORRESPONDENTS OF
ARCHIVES OF PEDIATRICS
Subscription $6.00 a Year, in Advance
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REPRINTS of articles appearing among
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change is permanent or temporary.
The Cardiac Transition of the
with Heart Block. Part II.
The Poison Cause of Poliomyelitis and Obstructions to its Investigation.
CONTENTS
ORIGINAL COMMUNICATIONS
Ascorbic Acid as a Chemotherapeutic Agent.
Newborn.
‘Continued on page 5)
W. J. McCormick, M.D.
Congenital Cardiac Dilatation
Jonn A. Freet, M.D.
A. Scopey, M.D.
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A Rational Complementary Therapy for Coughs
A nlosecm...... for cough sedation
Squibb Non-Expectorant Cough Sedative
A fruit-flavored preparation that depresses the
cough mechanism when sedation is essential.
In pints and gallons.
Per fluidounce:
Prophenpyridamine maleate. . . . . 25mg.
Codeine phosphate . . . . . 65mg.
for expectorant action
Squibb Expectorant for Coughs
A wild cherry-flavored preparation that pro-
duces an effective expectorant action when
cough is non-productive. In pints and gallons.
Per fluidounce:
Prophenpyridamine maleate 25 mg.
Ammonium chloride . . . 500 mg.
Ephedrine sulfate . . . . 75 mg.
SQUIBB
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(Continued from page 3)
DEPARTMENT OF ABSTRACTS
Rogers, H. M.: Disturbances of Cardiac Rhythm and Conduction in Con-
genital Cardiac Disease. Report of Five Cases
Manning, M. P., and Yu, P. N. G.: Electrocardiographic Changes in Polio-
myelitis. Analysis of 150 Cases
Tahka, H.: The Weight of the Thymus in Children of 0-2 Years of Age... .
(aunnarson, S., and Melin, K. A.: The Electroencephalogram in Enuresis. .
Fisher, B. M., et al.: The Subcutaneous Administration of the Sodium Salt
of Para-Aminosalicylic Acid in the Treatment of Tuberculosis
vhilds, D. S., and Kennedy, R. L. J.: Reticulo-Endotheliosis of Children’s
Auerbach, O.: Tuberculous Meningitis—Correlation of Therapeutic Results
with the Pathogenesis and Pathologic Changes. I. General Considerations
and Pathogenesis
Greenberg, M., et al.: The Relations Between Recent Injections and Paralytic
Poliomyelitis in Children
BOOK REVIEWS
Rx for Medical Writing. By Edwin P. Jordon, M.D., and Willard C.
Shepard
Dynamic Psychiatry. By Louis S. London, M.D
ITEMS
Risks of External Application of Penicillin
Oligophrenia Phenylpyruvica
CIVES EXCELLENT RESULTS
Cuts short the period of illness and relieves the
distressing spasmodic cough. Also valuable in
Bronchitis and Bronchial Asthma.
In four-ounce original bottles. A teaspoonful every
3 to 4 hours.
Extensively Used in Pediatric Practice.
GOLD PHARMACAL CO. NEW YORK CITY
4
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195
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It is donated by this publication in cooperation with the Advertising
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COMPLETENESS ... . All vitamins whose requirements have been estab-
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PALATABILITY . . . . Pleasant tasting in itself, DAPTA mixes readily with
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DAPTA
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MEAD JOHNSON & CO
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idequate carbohydrate to spare protein for its
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This classic caloric distribution is conven
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For over 40 years, milk and Dextri-Maltose
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Widespread clinical experience
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of milk in any form.
Steadily
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Cartose contains a mixture of carbohydrates—
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Added to the infant's formula,
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OINTMENT
the pioneer external
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“soothing, drying
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protective — Desitin Ointment
“showed definite prophylactic
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therapeutic — Desitin Ointment
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4 Desitin Ointment is a non-irritant blend of infections of the skin in the
newborn infant.
high grade, crude Norwegian cod liver oil (with its un-
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cum, petrolatum, and lanolin. Does not liquefy at body ; Az. e exanthema
temperature and is not decomposed or washed away 2 : e non-specific dermatoses
by secretions, exudate, urine or excrements. Dressings = e inte rtrigo o chafing
easily applied and painlessly removed. irritation
Tubes of 1 02., 2 02., 4 0z., and 1 Ib. jars.
: (due to urine, excrement,
write for samples and reprints : chemicals or friction)
DESITIN 1. Heimer, C. B., Grayzel, H. G., and Kramer, B.: Archives of
CHEMICAL COMPANY @ Pediat. 68:382, 1951
: a 2. Behrman, H. T., Combes, F. C., Bobroff, A. and Leviticus, R.:
70 Ship Street + Providence 2,R.1. | Ind Med & Surg. 18:512, 1949
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The NEW
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Note The standard dose of Bicillin, 1 teaspoonful, supplies 300 mg. (300,000 units).
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ARCHIVES OF PEDIATRICS
VoL. 69 APRIL 1952 No. 4
JOHN FITCH LANDON, M.D.. Editor
EDITORIAL BOARD
HAROLD R. MIXSELL, M.D., New York JOHN ZAHORSKY, M.D., St. Louis
REUEL A. BENSON, M.D., New York JOSEPH S. WALL, M.D., Washington
PHILIP M. STIMSON, M.D.. New York FREDK. H. WILKE, M.D., New York
ASCORBIC ACID AS A CHEMOTHERAPEUTIC AGENT
W. J. McCormick, M.D.,
Toronto, Canada
Until recently ascorbic acid has been used primarily and solely
for its vitamin action as an antiscorbutic agent. In such use the
daily requirement of the infant and young child has been placed
at 25 to 50 mg. and that of the adult at 75 to 150 mg. The vitamin
C properties, which are mainly prophylactic, are related primarily
to its role in maintaining stability and tensile strength of connec-
tive tissues generally, including the subcutaneous tissues, the mus
culature of the vascular and alimentary systems, and the osseous
tissues. This property favors the healing of wounds, the preven-
tion of hermorrhage and rupture of connective tissues, and the
building of a protective barrier against infectious invasion. Vitamin
C is also known to play an essential part in the oxidation-reduction
system of tissue respiration and to contribute to the development
of antibodies and the neutralization of toxins in the building of
natural immunity to infectious diseases.
Aside from these vitamin properties there is a very potent
chemotherapeutic action of ascorbic acid when given in massive
repeated doses, 500 to 1,000 mg., q.q-h., preferably intravenously
or intramuscularly. \When thus administered the effect in acute
infectious processes is favorably comparable to that of the sulfona-
mides or the mycelial antibiotics, but with the great advantage of
complete freedom from toxic or allergic reactions. The advantage
of parenteral administration is obvious when one considers that
the vitamin, being water-soluble and having no kidney threshold,
is eliminated by this route almost as rapidly as absorbed from the
alimentary system. By intensive parenteral therapy the blood level
131
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152) McCormick: Ascorbic Acid, a Chemotherapeutic Agent
can be maintained at a much higher degree of saturation with
resultant increase in antitoxic action.
The writer’ has previously reported spectacular results by this
method in the treatment of tuberculosis, scarlet fever, pelvic infec-
tion, septicemia, etc. Concurrently, by this same method, Klenner’
has reported dramatic results in the treatment of virus diseases,
including poliomyelitis, encephalitis, measles, herpes zoster, virus
pneumonia, etc.
This chemotherapeutic effect of ascorbic acid results from its
chemical action as a reducing or oxidizing agent. In fact the
decolorization of the test reagent, dichlorphenol-indophenol, is
dependent upon this property. By this means the viral or bacterial
toxins are rapidly neutralized and the febrile process, with its high
metabolic rate, is abated, usually within a few hours of the begin-
ning of treatment. Complete recovery occurs usually in a matter
of days. By this method the writer has been able to reduce marked
leukocytosis in purulent infections to normal within two or three
days. Likewise, Klenner* reports the reduction of pleocytosis of
spinal fluid in poliomyelitis to normal within 48 hours, under
intensive ascorbic-acid therapy. This reduction of leukocyte con-
tent of blood and spinal fluid is the best evidence of therapeutic
efficacy. Such effects have never been obtained by the use of
sulfonamides or mycelial antibiotics.
A point to be noted in this intensive method of therapy is that
the urinary elimination of ascorbic acid, being necessarily heavy,
is likely to cause confusion in case of urinary tests for sugar, since
ascorbic acid is an even more potent reducer of Fehling’s or Bene-
dict’s solution. Thus a positive test under these conditions does
not necessarily indicate sugar. This fact in itself is further evidence
of the efficacy of ascorbic acid as an oxidation-reduction agent.
Not only endogenous, but exogenous toxins are neutralized by
this chemotherapeutic action of ascorbic acid. By this means Klen-
ner has effected rapid recovery from rattlesnake bite in dogs, and
the author has obtained rapid recovery in a case of scorpion sting
by a single intravenous injection of 1,000 mg. Likewise, ascorbic
acid has been effectively employed in the treatment of lead poison-
ing* in painters, and in suppressing toxic reactions in sulfonamide’,
hormone, salicylate and arsenical therapy’.
Once the acute febrile or toxic stage of an infectious disease is
AL
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McCormick : Ascorbic Acid,a Chemotherapeutic Agent 153
brought under control by massive ascorbic-acid administration, a
relatively small maintenance dose of the vitamin will be adequate
in most cases to prevent relapses, just as in fire protection small
chemical extinguishers may be adequate to prevent fires in their
incipiency, whereas when large fires have developd water from
large high-pressure fire hose becomes necessary.
In determining the anti-infectious protective dosage of vitamin C
there is another factor which is not generally considered, When
the vitamin is employed to neutralize toxins of endogenous or
exogenous origin, the action is reciprocal in that the vitamin is
also neutralized proportionately, leaving less available for physio-
logical needs. To illustrate the writer has determined by laboratory
and clinical tests that the smoking of one cigarette neutralizes in
the body approximately 25 mg. of ascorbic acid, or the amount in
one medium-sized orange. It will thus be seen how difficult it is
to meet the bodily requirement of the pack-a-dav smoker for even
the protective level of vitamin C from dietary sources. It is thus
obvious that the steady smoker, who is usually short on his dietary
intake as well, requires much heavier therapeutic dosage of this
vitamin than the non-smoker. This may explain why, according
to Mayo-Clinic reports, the incidence of post-operative pneumonia
is four times greater in habitual smokers than in non-smokers. To
prevent post-operative pneumonia, Slotkin and Fletcher’ have
instituted the use of large doses of vitamin C both pre- and post-
operatively, with 100 per cent success. Prior to this innovation,
their post-operative pneumonia mortaliy rate was 20 per cent.
Pediatric surgeons might do well to follow this example. Klenner*®
reports that pneumonia never develops as a complication in measles
when intensive vitamin C therapy is employed early in the disease.
During the past century there has been a steady decline in the
incidence and mortality of most all infectious diseases. Epidemio-
logists generally* * ' admit that the control measures employed
“are not adequate in themselves to explain the recorded decline.”
“While the control measures which have been applied have prob-
ably accentuated the decline in young adult life . . . it seems reason-
able to attribute the general decline to other factors more general
in character and of which but little is really known.”
From increasing evidence of the antitoxic and anti-infectious
action of vitamin C, and from personal clinical experience in the
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prophylactic and therapeutic application of this vitamin, the author
is firmly convinced that the major factor in bringing about this
gradually changing picture in infectious-disease incidence has
heen the steady and phenomenal increase in the consumption of
vitamin-C-rich fruits, notably citrus fruits and tomatoes, during
the period in question. This hypothesis would not only account
for the gradual decline in incidence, but would also explain the
shift in age incidence of tuberculosis, diphtheria, poliomyelitis, etc.,
from the younger to the older age brackets, due to the fact that
in the nursery the full benefit of this nutritional reform is obtained ;
whereas, during childhood and early youth perverse dietary habits
are gradually acquired through lack of parental guidance and
inadequacy of public-health education. The increased use of candy,
carbonated beverages, tea, coffee, tobacco and alcohol tends
gradually to displace the more wholesome nutritional habits of
early childhood, and malnutrition with increased susceptibility to
clisease is the price we pay for this diversion,
In conclusion it may be of interest to note that centuries ago
observing physicians detected the predisposing influence of scurvy
on the incidence of infectious diseases. In 1689, Richard Morton,
one of the earliest writers on tuberculosis (then known as
phthisis ), states in his famous “Phthisiologia” that “scurvy is wont
to occasion a consumption of the lungs.” Likewise, Boerhaave, a
Dutch physician of international repute in the early 18th century,
held to the view that “gangrenous gingivitis,” then frequently con-
current with diphtheria, was evidence of a scorbutic background.
MMARY
Clinical and laboratory evidence is cited in support of the
author's advocacy of intensive vitamin C administration as a
chemotherapeutic agent in infectious dieases.
The efficacy of this therapy is dependent upon the potent
oxidation-reduction action of ascorbic acid and the use of massive
doses with complete freedom from toxic or allergic reactions.
There is an unusually broad spectrum of antibiotic action in
this therapy, including practically all bacterial and viral infections
It is also highly potent as an antitoxic agent in exogenous poison-
ing, organic and inorganic.
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REFERENCES
McCormick, W. J] Vitamin C in the Prophylaxis and Therapy of Infectious
Diseases. Arcu. Pepiat., 68: 1-9, 1951
Klenner, Fred R.: Massive Doses of Vitamin C nad the Virus Diseases. Paper
presented at convention of the Tri State Medical Association of the Carolinas
and Virginia, held at Columbia, Feb. 19-20, 1951
Klenner, Fred R.: The Treatment of Poliomyelitis and Other Virus Inseases with
Vitamin C. South. Med. & Surg., Vol. IIT, No. 7, 199
Holmes, H. N.; Campbell, K. and Amberg, E. J Effect of Vitamin C or Lead
Poisoning. J. Lab. & Clin. Med., 4: 1119, 1939.
McCormick, W. J.: Sulionamide Sensitivity and C-Avitaminosis. wnad, M.A.J.,
52: 68-70, 1945
Pelner, L Use of Ascorbic Acid in Reducing Toxicity of Stilboestrol and
Arsenical Therapy. J.A.M.A., 123; 112, 1943.
Slotkin. G. A. and Fletcher, R. S:; Ascorbic Acid in Pulmonary Compheations
Following Surgery. J Urol... Nov. 6, 144
A Tuberculosis Mortality in Ontario. Canad Pub. Health J., 25:
73, 1934.
McKinnon, N. E.: Mortality Reductions in Ontario, 1990-1942, Canad Pub. Health
J., 36: 423, 1945.
Davis, Paul V.: Tuberculosis Epidemiology. Dist. of Chest, p. 21, Sept. 1939
16 Gothic Avenue.
Risks oF ExTeRNAL APPLICATION OF PENICILLIN, (Presse
Medicale, Paris, 59: 713, May 23, 1951). In 32 (14 8%) of
215 patients with medicamentous dermatitis, the eczema was
caused by the local application of penicillin, Seven cases are re-
ported in detail. Eye lotions containing penicillin caused intoler-
ance to the antibiotic in six instances, penicillin dusting powder im
two instances, and penicillin creams in 19 instances. In three
patients who had been treated with penicillin cream for sycosts
of the beard, for ulcer of the leg, and for an insignificant skin lesion
respectively, resulting sensitization prevented continuation of gen-
eral penicillin treatment, which was indicated for a furuncle of the
upper lip, pneumonia, and syphilis, respectively. The cutaneous
sensitization may entail general sensitization, which contraindicates
penicillin treatment by parenteral route in cases of severe infection
in which this treatment is imperative. Considering these facts
jointly with the risk of penicillin resistance, the abuse of local peni-
cillin therapy must be condemned, because there are no cases ot
pyodermatitis, superinfected dermatosis, accidental skin lesions,
conjunctivitis, or rhinopharyngeal or buccal lesions that could
not be treated with other antiseptics without jeopardizing the
recovery of the patient. The same moderation that has been ad-
vised concerning local sulfonamide therapy is urged with respect
to the local administration of powerful antibiotics.—Journal
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THE CARDIAC TRANSITION OF THE NEWBORN
CONGENITAL CarpIAcC DILATATION WitTH HEART BLOCK
REPORT OF CASE
Joun A. Freer, M.D.
Bay City, Mich
Part I]
~ Family History. The father, essentially negative. The mother
was a white, obese woman, age 33. For the past seven years
she has been a diabetic. During the entire time of this pregnancy
she was sugar free, being controlled both by diet and insulin.
She was a para VIII. Previous deliveries, five normal, two
muscarriages.
Medication during labor, ether with pains only. Because of
uterine initia, after complete dilatation of the cervix, she was
given 2 min, of obstetrical pituitary. She delivered twelve minutes
later.
examination during labor showed the position of the fetus to be
l.. O. A. Fetal heart tones were good, and varied between 120
and 132 beats per minute.
A female infant was born December 19, 1950. The birth weight
was 10 pounds 42 ounces. The birth length was 20% inches.
No trouble was experienced with the infant at time of birth.
Baby's respirations were spontaneous. and the baby’s bronchial
tubes contained very little mucus. Its ery at birth appeared normal.
Shortly after being taken to the nursery the baby developed
evanosis. It was given oxygen and placed in an incubator where
the oxvgen could be given continuously. The respirations were
rapid, and examination of the baby’s heart at that time revealed
no murmurs \ clinical diagnosis of enlargement of the heart
could not be made at that time, due to the difficulty in percussion
of the newborn's heart. Breast sounds were normal throughout
the chest, and the possibility of atelectasis was ruler out. The
cvanosis became less with the continued administration of oxvgen
Qn the second day of life, the Rh factor was taken, and found
to be positive, to antiserum Rho (Anti-D) Hemoglobin was 125
per cent. The red blood count was 6,040,000. Baby's weight, 9
pounds 3 ounces
The baby took water very poorly, and was unable to take
formula. The effort of nursing caused the respirations to become
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irregular, and there were twitchings of the muscles of both upper
and lower extremities. The hemoglobin was 140 per cent, and
the red blood count increased to 7,310,000. An x-ray of the chest
was ordered, with the following report: “The chest showed both
lung fields to be aerated satisfactorily. The cardiac shadow was
somewhat larger than usually seen, and its contour suggests a
congenital heart disease.” ( Fig. 1).
Fig. 1. Physiological dilatation of the heart. Cardiac shadow enlarged
in all diameters. Ratio of increase in diameters out of proportion to
heart later mm imtancy
Treatment, Routine care; Synkamin, 2 mg., intramuscularly.
The baby still unable to nurse, taking water poorly. Attempted
feeding with the lavage tube was a failure, as the baby showed signs
of collapse during this procedure. Feedings were then given with
an eye-dropper, placing the milk on the back of the tongue, and
allowing the baby to swallow.
The baby had several attacks, during the day, of cardiac col-
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lapse. During these attacks the baby had generalized severe
sweating, a high temperature, from 104° to 105° F., and convul-
jjons. The baby’s elimination was normal. No abnormalities
noted in urination or im the stools.
The weight of the baby on its third day of life, 9 p winds 8 our:ces.
taby's condition serious.
On the fourth day of life, the infant was very cyanotic, and its
condition poor, The baby was not removed from the incubator
for weighing or for bathing because of its critical condition. The
infant was given 10,000 U. penicillin, intramuscularly, daily, as 4
prevention against pneumonia.
During the day the infant had several spells which consisted
of high temperature, severe sweating and convulsions, irregular
respirations, and a weak and slow pulse. During these attacks the
haby was given a soda retention enema at room temperature to
replenish fluids and bring down temperature, and Metrazol 1 cc.
was given intramuscularly. Examination during attacks revealed
no murmurs of the heart, but the heart sounds were weak and
irregular. Examination of the abdomen revealed no findings, there
was no distention, and the peristohic sunds were normal. Liver
margins within normal limits. There was no yvoniting.
Phroughout the morning of the fifth day of life, the baby's
condition remained critical, though there had been no attacks since
> A.M. Examination of the abdomen at 10:45 A.M. revealed the
baby’s condition and findings to be the same as on the previous
dav. At 11:45 A.M., one hour after examination, the baby started
crying vigorously, cyanosis disappeared, and the baby took two
ounces of formula without any trouble. Examination of the infant
suggested the heart to be smaller on percussion, there were no
murmurs, and the rate, rhythm and heart sounds appeared normal.
Phe baby was placed on routine care and feeding, but kept in the
incubator with continuous oxygen.
On the sixth day of life, the baby appeared very much improved
The baby’s morning weight was & pounds 14 ounces. Temperature,
Ox6° KF. The stool was suddenly loose and yellow. The baby
continued to sweat heavily when erying or during bowel move-
ments. Between 8:00 A.M. and 12:00 midnight, the baby's
temperature increased to 105. F., though its ery was normal, and
its cvanosis was very shght. There was general profuse sweating.
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but there were no convulsions. There were only twitchings of
the legs and arms during these mild attacks.
On the seventh day of life, the temperature had returned to
O8° F, by 6:00 A.M. The infant was taking water very good, and
taking its formula with ease. The baby took three ounces at each
feeding. The stools regained their normal contour. At 12:00 noon
the temperature slowly returned to normal, During this time there
was moderate sweating, and weak tremors only present when the
baby cried.
Fie. 2. Diameters of heart decreased Cardiac shadow, bulbous. Supra
cardiac shadow, widened
On the eighth day of the baby’s life, the morning weight was
8 pounds 14 ounces ; hemoglobin 130 per cent, R. B.C., 5,460,000.
The baby’s highest temperature during this day was 102° F., and
that was at noon to 4:00 P.M. It dropped to normal during the
night. There were no attacks. Sweating and slight tremors of
the extremities were present only when the baby cried.
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On the ninth day of life, the baby’s condition was satisfactory.
Its weight was 9 pounds 2 ounces, and the temperature throughout
the day only varied from 98.6° to 99.4° F. The baby was taken
out of the incubator, and the oxygen discontinued. From the
tenth to the fourteenth day of life the baby made gradual improve-
ment with the disappearance of all symptoms, and with normal
gain in weight. The daily injections of penicillin were stopped
on the fourteenth day of life. On the fifteenth day of lite the
baby appeared normal in all respects. The baby’s weight was 9
pounds 14% ounces. An x-ray of the chest was taken on this day
with the following report: “Check-up studies of the chest do not
show any definite x-ray evidence of pathology at this time.” (Fig.
2). The infant was discharged, and taken home by mother.
At three weeks of age the baby’s weight was 10% pounds;
length, 22'3 inches. Physical examination—infant apparently
normal. Heart—no murmurs, rate and rythm normal; heart
sounds normal. Formula—powdered milk. The baby was given
cod liver oil; orange juice.
\t six weeks of age the baby’s weight was 1112 pounds; length,
22', inches. Formula—powdered milk. Baby given cod liver
oil, orange juice, cereals and puddings. Physical examination
haby appeared normal throughout.
(ine week later, the mother brought the baby to the office with
the complaint that the baby had a cold and a temperature. Physical
examination—general appearance, acutely ill. Color, no cyanosis
normal. Head examination—throat red, large amounts of post-
nasal discharge. Cervical glands enlarged. Chest—the heart, on
percussion, showed no enlargement. There were no murmurs
present, though the rate was rapid. Lungs—rales and wheezes
throughout the bronchial tree. Remainder of examination, neg-
itive
Diagnosis. Nose and throat infection, bronchial pneumonia.
Treatment. Routine care. Penicillin, water soluble, 50,000 U
tablets given every four hours, night and day. At no time did
this infant show any signs of cardiac or circulatory failure, and
at no time could its condition be considered critical. It was pro
nounced completely cured clinically, within ten days.
Check-up at eleven weeks of age. Weight, 12% pounds; length,
23!'4 inches. Physical examination-—no findings bearing from the
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normal. Formula—powdered milk. Baby continued on cod liver
oil, fruit juices, cereals, puddings, and strained vegetables and
meats were added.
At three months and one week of age the baby was brought to
the office, the mother stating that the baby was suffering a loss
of appetite, and a low-grade temperature in late afternoons and
nights. Examination revealed a recurrence of the throat infection,
Fie. 3. Heart within limits of normal. Cardiac and supracardiac
shadows are widened on both sides. Note scattered areas of increased
density in lung tissue.
and scattered rales throughout the bronchial tree. The baby’s
heart rate was increased, but, otherwise, was considered normal.
An x-ray of the chest at this time showed a bilateral lobular
pneumonia, infiltration from moderate to severe. The upper
mediastimun was considered normal, and. as much as the chest was
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in midrespiratory phase, the heart was considered normal (Fig. 3).
Diagnosis. Wilateral lobular pneumonia,
Vedication. Water soluble penicillin given orally; selective
diet continued. The baby’s recovery was uneventful.
Five months of age check-up: Baby's weight, 1434 pounds;
length, 251% inches. At this time the baby’s condition appeared
very good. Physical findings were all within normal. The baby
was kept on a selective diet which was fortified by vitamin therapy.
Roth cardiac and supracardiac shadows are widened to
Note decreased areas of density in lungs
In five months a progress X-ray was taken. Report: The heart
appeared normal. The hospital roentgenologist made a diagnosis
of virus pneumonia when shown the film. This I could not agree
with, as the patient at that time appeared normal, clinically. No
temperature. Throat and nose normal, and chest appeared normal.
| feel that the scattered areas of increased density, resembling the
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pathology of virus pneumonia, are due to changes in the lung
tissue from previous attacks of pneumonia (Fig. 3).
Nine months of age check-up: Baby's weight, 16 pounds ; height,
2734 inches. Head and neck, apparently normal. The baby had
no teeth present at nine months, though the gums gave the impres-
sion that the incisors were attempting to cut through. Nutrition,
good, Chest, clear. No rales or wheezes. Heart appeared normal.
No murmurs. Abdomen, no tenderness or muscle spasm. Liver,
on percussion and palpation, was within normal limits. Extrem-
ities appeared normal. Reflexes normal.
On history, mother stated baby’s hands and feet became cold
and a little blue while sleeping. No other signs of fatigue or
cyanosis. Baby plays with his brothers and sisters, stands in
playpen, and walks if supported.
Progress X-ray. Report: “Heart within limits of normal. There
are still many patches of increased density throughout the chest.
These areas are considerably less than in the previous X-ray”
( Fig. 4).
DISCUSSION OF BABY AT TIME OF BIRTH
Diagnosis. Transient dilatation of the heart with partial heart
block.
Etiology. Metabolic toxins transmitted to the infant, from the
blood stream of a moderately advanced diabetic mother.
Symptoms. This baby at birth weighed 10 pounds 44% ounces.
It was much overweight for a baby at term. The mother, being a
diabetic, a large baby should be expected, as being overweight at
birth is characteristic of babies of diabetic mothers. The degree
of diabetes suffered by the mother apparently plays little part in
the weight of the infant at birth, as the infant is usually large.
It makes no difference whether the diabetes is mild or severe.
Cyanosis. The most common causes of cyanosis in the newborn
are asphixia, and heart disease. With asphixia the infant, as a
rule, is cyanotic at birth. In heart disease, the infant usually
develops cyanosis shortly after birth, as happened in this case.
Rh Factor. A positive Rh factor does not always spell disaster
for the infant. Many infants are born with a positive Rh factor
and are never diagnosed, as they never give any clinical evidence
of the disease. There was no jaundice or any clinical evidence
that the Rh factor was contributing to the infant's condition, so
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the infant was watched closely, and no treatment given for this
condition,
Blood Count. Though the hemoglobin was 125 mg. per cent,
and the red blood count 6,040,500 red cells per cu. mm., and during
the course of the acute condition rose to between seven and eight
millon R. B.C. per cu. mm., it cannot be stated that the blood
count was diagnostic of congenital heart disease in the infant. In
congenital heart disease, caused by congenital defects, the red
blood cells will rise to between ten and fourteen thousand R.B.C
per cu. mm. of blood. Due to the fact that the red cells increase
in order to provide oxygen to the tissues of the infant, and this
baby was kept continuously in an incubator that gave it a high
concentration of oxygen, may account for the relatively low red
blood count in this baby with cyanosis and a dilated heart. It is
hard to make an exact statement of what the blood count is in
the newborn, as it varies all the way from five million to over six
million R.B.C. per cu. mm. of blood at the time of birth. These
are the figures that are found in the literature on this subject.
Loss of Appetite. The failure to nurse by this infant during its
first week of life was not a true loss of appetite, but rather failure
to nurse because of fatigue and weakness brought on by the physical
exertion of nursing. This baby was hungry, and would start to
nurse, but after one to two minutes of nursing, it would become
weak, begin to sweat, cyanosis would increase, and it would start
twitchings of the extremities. The pulse would slow, and respira-
tions would become shallow. These symptoms also repeated them-
selves during crying.
Dilatation and Heart Block. As both dilatation of the heart
and a heart block were present in this infant it was difficult to
ascertain, during these attacks of collapse in the first four days of
the baby’s life, a true picture of the symptoms and signs of either
condition. The signs and symptoms of the heart block could have
heen superimposed upon the signs and symptoms of the dilated
heart. It could also be argued that the heart block caused the
transient dilatation of the heart.
It is my opinion that the heart block was present from birth,
and that the auricles were not contracted during cardiac transition,
hecause the heart block mechanically impeded this action, Though
the specialized tissue of the heart was depressed by the toxins in
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the infant’s blood stream, the heart block manifested itself clinically
in irregular paroxysms.
The infant is born with the auricles dilated and filled with
blood. With the presence of the irregular and independent rhythm
and rate of the auricles and ventricles, the auricles emptied the
blood contained irregularly, and in smaller volume into the ven-
tricles. Thus the blood could not be equalized, or placed in balance
among the four chambers of the heart, with the resultant, transient
dilatation. As the rate and rhythm of the auricles and ventricles
became more synchronized, the transition or contraction of the
auricles took place.
\fter the contraction of the auricles took place, the heart block
persisted and did not disappear for a number of days. After this
dilatation corrected itseli the attacks of syncope became less fre-
quent and less severe until they completely disappeared.
CONGENITAL DILATATION NEWBORN HEART
OF THE
I do not believe that this condition was an acute dilatation of
the infant’s heart. As stated several times in this manuscript, the
infant's heart is dilated before birth, due to the increased size of
the auricles. The immediate transition of contraction of the heart
muscle was delayed until the fifth day. I refer to this as a transient
dilatation or a dilatation which is nothing but a continuation of
the size of the fetal heart at term, especially the size of the auricles.
3y this I do not mean that the entire heart of the newborn
had the same physiology as it had before birth. Most of the
transition of the heart had taken place. There is only a failure of
full contraction of the auricles. The pulmonary circulation had
been established. The beginning of the closure of the ductus arteri-
osis and the ductus venosus had taken place. The foreman ovale
had closed. The failure of the auricles to establish a greater systole
and a lesser diastole, however, limited the amount of blood that
they furnished the ventricles. For this reason, the ventricles of
the heart were functioning on decreased volume and rate of flow
of the blood.
It is also my contention that these toxins could account for the
failure of contraction of this newborn's heart.
Some readers of this paper may conclude that the “All or None
Law” of cardiac muscle contraction and relaxation has been vio-
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lated. ‘Lo this | wish to state that we all know that heart muscle,
when stimulated to contraction by either a weak or strong stimull,
contracts and relaxes to its maximum. While keeping the “All
or None Law” of heart muscle in mind, we must not forget, that
the extent of a maximum contraction or dilatation is dependent
upon mechanical factors. These are first, the volume of blood in
each chamber for its muscle to contract on, and second, the rate
of flow or velocity of the blood in refilling these chambers.
It is apparent that the heart has the ability to adjust its maximum
contraction and dilatation to the volume of blood present in its
chambers
(me theory claims that dilatation is brought about by the blood
entering the heart chamber and filling it to its maximum capacity.
To me, this is not the major cause of dilatation. Heart muscle,
like other striated muscle, in its period of relaxation, dilates rapidly
at the end of contraction, then in a pendulum action tries to equal
the force and duration of the contraction.
lurther, | contend that dilatation may be stimulated in its action,
in a sinnlar manner to contraction. If this were not true, then
how could we account for auricular diastole being greater than
auricular systole in the fetal heart? The strength of systole alone
does not account for the force and duration of diastole in the heart.
In this case, it is my opinion that the transient dilatation was due
indirectly to the toxins of diabetes in the mother. Assuming that
the heart block was present from birth, it is easy to see how the
auricles, beating faster than the ventricles, would cause a damming
back of the blood in the right auricle, and even in the left auricle.
causing an increased volume in the auricles. This would cause
a marked embarrassment of both thepulmonary and the systemic
circulations. As the toxins were eliminated by the excretory systems
of the infant, the heart block became less severe. The rate of the
ventricles increased, and the auricles allowed to empty more blood
into the ventricles, with the resultant contraction of the auricles
to their neonatal normal.
With this hypothesis, the signs and symptoms present in this
case, and the progress and disappearance of the symptoms cor-
respond perfectly with the physiological pathology presented,
Phe type of heart block present was that which could be ac-
counted for as originating in the auricularventricular node. The
symptoms expected would be convulsions and coma, due to lack
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of blood and oxygen to the brain. The severe sweating during
attacks and high temperature that were carried by this infant are
also accounted for by auricularventricular heart block.
Cyanosis and fatigue are symptoms of cardiac dilatation.
HEART BLOCKS
There are many different diseases and conditions that will
produce a blocking of the impulses in the conduction system of the
heart. In this manuscript we are only interested in one type.
That is the congenital heart block of the newborn. Congenital
heart blocks are caused either by the effect of toxins upon the
conduction system, or by anatomic deformities in the bundle of His.
The chief anatomical deformity producing heart block is a patent
interventricular septum.
Heart blocks caused by toxins may be either caused by toxins
absorbed from the mother, such as in the case of a diabetic mother,
or by infections which the mother suffers at the time of delivery.
The symptoms of congenital heart block are first, attacks of
syncope, and these attacks may be accompanied by convulsions
or twitchings. Twitchings occur only when there is a prolonged
standstill of the ventricles, with the failure of the ventricle to
furnish sufficient blood to the cerebral circulation. Heart blocks
are also occasionally caused by the toxic absorption of the digestive
system of the newborn, but this type usually develops within a
period of time after birth, and is never present at the time of birth
or within the first week of life. Cyanosis is not the symptom of a
partial heart block or of the type which I feel was present in this
infant. Generalized and profused sweating during the time of
attacks, which is a diagnostic symptom of heart block, was present,
and to a marked degree.
Nystagmus may be a symptom of heart block in older children.
I do not feel that it is too diagnostic in the newborn. The eyes
of this infant were watched during attacks, and the only abnormal
movements that were made were that the eyes were drawn upwards
and more or less fixed. This symptom of heart block is possibly
complicated by the lack of coordination of the muscle of the eye
at birth.
Because these symptoms of heart block just presented were
present during attacks and gradually became weaker until they
finally disappeared, and due to the fact that up to the ninth month
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168 FrEEL: Cardiac Transition of Newborn
of age these attacks have never recurred, it could not be stated
that they were due to a deformity in the conduction system, or
heart. The only logical explanation is diabetic toxins present in
the infant’s blood stream at time of birth.
FAILURE OF TRANSITION
Failure of transition of the newborn's heart can be due to either
anatomical or physiological pathology, or to a combination of these
factors. Anatomical failure can be due to defects, either in the
heart, or blood vessels leading to or going away from the heart.
The failure of the physiological factors of transition can be moti-
vated either by intrinsic or extrinsic factors.
ABNORMALITIES IN THE TRANSITION OF THE NEWBORN’S HEART
IN THE CASE PRESENTED
The only abnormality that can be detected in this case is first, a
prolonged dilatation of the heart, particularly the auricles ; second,
a disturbance in the conduction system, in the auricularventricular
node, causing an auricularventricular block with frequent attacks
of paroxysms of bradycardia. This disturbance in the auricular-
ventricular node was motivated by the products or toxins of the
body of the diabetic mother. These toxins can be either a single
toxin or toxins from the metabolism of the diabetic mother’s body,
or the effects of these toxins upon the tissues and fluids of the
mother’s body or the effects on the newborn’s body.
It is known that the toxins from bacterial growth or from
metabolic diseases can set up a chemical reaction with the protein,
fats, or carbohydrates of the body tissues or fluids, causing by-
products that are more toxic than the original toxins themselves.
Further evidence of the toxins of diabetes affecting the auricular-
ventricular node, causing partial heart block, can be found in the
adult, for one often finds this condition in many cases of uncon-
trolled diabetes. Apparently, these toxins have weakened the
sensjtivity of the auricularventricular node to such an extent that,
when the auricular excitation waves come into contact with the
auricularventricular node, they fail to stimulate the ventricles to
contraction.
As the infant’s body eliminates these toxins, the auricular con-
tractions are more regularly carried into the ventricles and cause
bad
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the heart block to gradually disappear. After a period of days
the ventricular beat becomes normal.
The periods of auricularventricular block, in this case, became
less severe and farther apart until they disappeared. The infant
at nine months of age has showed neither signs nor symptoms of
dilatation or heart block. It is hard to deny that the toxins from
the metabolism of the diabetic mother’s body played a very big
part in the etiology of this condition,
IM PRESSION
The heart of the newborn goes through a definite pattern of
transition from intra-uterine life to extra-uterine life. This transi-
tion consists both of anatomical changes and functional or physio-
logical changes. The chief anatomical changes are: ;
1. Obliteration of the umbilical arteries and veins.
2. Closure of the ductus arteriosus and ductus venosa.
3. Closure of foreman ovale.
4. Contraction of the heart to a smaller size than before birth
at term. This change in size consists of the contraction of the
muscles of the heart of the newborn, especially those in the auricles.
Physiological changes are :
1. Cessation of placental circulation.
2. Decrease in blood volume.
3. Establishment of pulmonary circulation.
4. Increase of pressure in systemic circulation.
5. Changes in the pressures of the force pump action of the
heart. That is, the fetal heart at term must change from a greater
negative pressure and a lesser positive pressure to a greater positive
pressure and a lesser negative pressure after birth.
SUMMARY OF CASE PRESENTED
1. The newborn infant’s mother had a history of controlled,
moderately advanced diabetes mellitus.
2. The delivery was spontaneous, and all aspects of the birth
normal.
3. Infant overweight at birth.
4. Development of cyanosis within one hour after birth. Later
there appeared lethargy, coma, convulsions, and high temperature.
These are all signs of cardiac dilatation in the infant.
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170 FreeL: Cardiac Transition of Newborn
5. The appearance of cardiac collapse, with slow and weak pulse.
These were attacks of syncope with generalized, severe sweating.
It was on the third day of life that the diagnosis was made of
the heart. This condition may have been present since birth, but
auricularventricular heart block is difficult to diagnose in the new-
born, clinically. It could have been diagnosed with an electro-
cardiogram. The baby’s condition became gradually and progres-
sively worse until after the fifth day of life. After the sixth day
of life the symptoms of dilatation gradually disappeared.
6. Attacks of the auricularventricular heart block became more
frequent and severe until the eighth day of life when they began
to lessen, both in severity and occurrence, and were absent at the
time of discharge on the fourteenth day of the infant's life.
Treatment. Absolute rest, mechanical feeding, Metrozole during
attacks, and penicillin to prevent pulmonary infections, enemas to
remove toxins from gastrointestinal tract, and retention enemas,
if possible, for dehydration.
CONCLUSION
1. This case presents a failure of the prolonged immediate transi-
tion of the muscle of the newborn heart.
2. A heart block was caused by the effects of extrinsic toxins
(diabetic toxins absorbed from mother) upon the atrioventricular
node.
3. Failure of the completion of the transition of pressures of
the heart. That is, a failure of the transition from a greater neg-
ative pressure and lesser positive pressure in the fetal heart at
term to a greater positive pressure and a lesser negative pressure
in neonatal life.
4. Incidence. In reviewing the literature, it is claimed that
both cardiac dilatation and auricularventricular heart block are
both rare findings in the newborn.
I feel that both of these conditions are more common than
thought, as infants with these conditions can recover or die while
under treatment for some other pathology present, or go unnoticed
by a mistaken diagnosis.
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COM MENTS
The views and ideas expressed in the classification and explana-
tion of the physiology of the transition are purely my own. It is
practically impossible to get first hand information by direct obser-
vation of the living heart of the human fetus interutero. For this
reason the deductions made here on the action of the heart as a
force pump were obtained by applying the laws of physics of
fluids and of the force pump.
[ do not present these ideas as theories or fact, but as a hypoth-
esis that is a very likely, and a possible explanation of this physio-
logical phenomena which at present is very poorly understood.
References are cited throughout this manuscript where | felt
reference was necessary. For statements which I felt were general
knowledge, no notations or bibliography are given.
Center Avenue.
OLIGOPHRENIA PHENYLPYRUVICA. (Medical Journal of Aus-
tralia, Sydney, 1: 761, May 26, 1951). In phenylpyruvic oligo-
phrenia, described in 1934 by Folling of Oslo, mental deficiency
is associated with the excretion of phenylpyruvic acid in the urine.
The acid is easily detected by the addition of liquor ferri perchloridi
to the urine. The excretion of this acid is the result of faulty
metabolism of the product of the digestion of protein, the amino
acid phenylalanine. Phenylpyruvic oligophrenia is hereditary and
is transmitted by a single gene. A survey of 1,520 mentally de-
fective patients in Norway revealed 23 patients with phenylpyruvic
oligophrenia, and also disclosed that a high degree of consanguinity,
such as the marriage of first cousins—if they carried the causa-
tive recessive gene—resulted in a higher familial incidence of the
malady. The gene influences the nervous system through the
phenylalanine-derived toxin, and mental deficiency results. Tremor,
muscular rigidity, active deep reflexes, and athetosis may some-
times be noted. Cantor’s aim was to call attention to this dis-
order. He will describe in a later report the three cases of pheny!l-
pyruvic oligophrenia that have been found in Victoria. He sug-
gests that other mentally defective patients should be surveyed for
excretion of phenylpyruvic acid.—Journal A.M.A.
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THE POISON CAUSE OF POLIOMYELITIS AND
OBSTRUCTIONS TO ITS INVESTIGATION*
R. Scopey, M.D.
Syracuse, N. Y.
The disease that we now know as poliomyelitis was not desig-
nated as such until about the middle of the 19th Century. Prior
to that, it was designated by many different names at various times
and in different localities.’.* The simple designations, paralysis,
palsy and apoplexy, were some of the earliest names applied to
what is now called poliomyelitis.
Paralysis, resulting from poisoning, has probably been known
since the time of Hippocrates (460-437 B.C.). Boerhaave,’ Ger-
many, (1765) stated: “We frequently find persons rendered par-
alytic by exposing themselves imprudently to quicksilver, dis-
persed into vapors by the fire, as gilders, chemists, miners, etc.,
and perhaps there are other poisons, which may produce the same
disease, even externally applied.” In 1824, Cooke,‘ England,
stated: “Among the exciting causes of the partial palsies we may
reckon the poison of certain mineral substances, particularly of
quick silver, arsenic, and lead. The fumes of these metals or the
receptance of them in solution into the stomach, have often caused
paralysis.”
Colton’? (1850) mentions the case of a patient who swallowed
some arsenic accidently and was admitted to the hospital. The
primary effects of the poison had been successfully combatted with
proper remedies, but seven days afterward he became paralyzed.
It is significant to note that there was a latent period of several
days before the paralysis appeared since this delayed reaction is
comparable to the incubation period in infectious diseases.
Vulpian® (1879) experimentally produced paralysis of the ex-
tensor muscles of a dog by lead poisoning. The lesions, consisting
in colloid degeneration and cell atrophy of the anterior horn cells
of the spinal cord were pronounced by Vulpian as poliomyelitis.
Adamkiewitz’ (1879) reported two parallel cases, one of polio-
myelitis and one of lead poisoning.
In 1881, Popow* of St. Petersburg, published an essay upon the
pathological anatomy of arsenical paralysis as produced artificially
in animals. The work of Popow was carried out under the guid-
*Statement prepared for the Select Committee to Investigate the Use of Chemicals
in Food Products, United States House of Representatives, Washington, D. C.
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Scosey: Poison Cause of Poliomyelitis 173
ance of the distinguished neurologist and microscopist, Professor
Mierzeyeski. Popow concluded that arsenic, even in a few hours
after its ingestion, may cause acute central myelitis or acute polio-
myelitis.
During an epidemic of poliomyelitis in Australia in 1897, Alt-
man* pointed out that phosphorus had been widely used by farmers
for fertilizing that year. This observation may be of significance
since in recent years organic phosphorus insecticides, such as
parathion, have been suspected as possible causes of poliomyelitis.
Onuff'® (1900) reported a case of a painter with flaccid paralysis
of both legs, in whom the autopsy showed lesions characteristic
of poliomyelitis.
Obrastoff" (1902) reported a case of acute poliomyelitis result-
ing from arsenic poisoning. Phillippe and Gauthard’ (1903) re-
ported a case of anterior poliomyelitis from lead poisoning.
Gossage’ (1902), writing on infantile paralysis, says: “The
nerve cells or fiber may be acutely disabled by the action of some
poison circulating in the blood, and it is possible that such poison
would only temporarily impair their functions or so seriously af-
fect them that recovery would be impossible.”
Dr. David E. Edsall'* (1907), writing on the pathology of car-
bon monoxide poisoning in Osler’s System of Medicine, states:
“Peripheral neuritis had repeatedly been described and _polio-
myelitis and disseminated encephalitis have been seen.”
Collins and Martland® (1908) reported a case of poliomyelitis
in a man, 38 years of age, which resulted from the use of potassium
cyanide as a silver polish. The illness began with diarrhea, fol-
lowed by headache and pain and stiffness in the back of the neck.
About eight days after the onset of the illness, he became paralyzed,
In discussing Collins and Martland’s paper, Larkin stated that he
had seen one instance of this disease following potassium cyanide
poisoning.
Collins and Martland poisoned several rabbits with potassium
cyanide and found pathological lesions in the spinal cord similar
to those found in cases of poliomyelitis.
In the spring of 1930, there occurred in Ohio, Kentucky, Ala-
bama, Mississippi and other states an epidemic of paralysis.’* "
The patients gave a history of drinking commercial extract of
ginger. It is estimated that at the height of the epidemic there
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174 ScosEy: Poison Cause of Poliomyelitis
were about 500 cases in the Cincinnati district alone. The cause
of the paralysis was subsequently shown to be triorthocresyl phos-
phate in a spurious Jamaica ginger. Death resulted not infre-
quently from respiratory paralysis similar to the bulbar paralysis
deaths in poliomyelitis. On pathological examination, the anterior
horn cells of the spinal cord in these cases showed lesions similar
to those of poliomyelitis.
These incidents show that epidemics of poisoning occur and,
furthermore, that epidemic diseases do not always indicate that
they are caused by infectious agents. Moreover, following the
ingestion of the spurious Jamaica ginger, the symptoms appeared
two to ten days later. In some cases a longer time elapsed. This
latent period is comparable to the incubation period of infectious
diseases. As a matter of fact, the incubation period of polio-
myelitis is commonly stated to be seven to 10 days on the average
with considerable variation in either direction. The so-called in-
cubation period in poliomyelitis and the latent period in these cases
of poisoning, therefore, are strikingly similar in length.
Leenhardt et al.’* (1951) described acrodynia in the course of
three cases of acute poliomyelitis. Some authorities have consid-
ered acrodynia to be caused by a poison. Elmore’’ (1948) re-
ported two cases of this disease following the ingestion of mercury
and Warkany and Hubbard* (1951) found mercury in the urines
of 38 (92.7 per cent) of 40 acrodynia patients. Meyerhofer*
(1939) reported that infantile acrodynia may immediately follow
certain forms of atypical poliomyelitis, especially encephalomyelitis.
Mercury is used as an insecticide and a fungicide and the above
clinical observations indicate that it might be a factor in producing
some cases of poliomyelitis.
Gougerot™ (1935) reported that during arsenical therapy for
syphilis, poliomyelitis developed in two patients, and lethargic en-
cephalitis followed by Parkinson’s disease in one.
In 1936, during a campaign to eliminate yaws in Western Samoa
by the injection of arsenicals, an epidemic of poliomyelitis ap-
peared simultaneously.” In one community all of the patients de-
veloped paralysis in the same lower limbs and buttocks in which
they had received the injections and this pattern was repeated in
37 other villages, whereas there was no paralysis in uninoculated
districts. The natives accused the injections as the cause of the
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Scosey: Poison Cause of Poliomyelitis * 175
epidemic of poliomyelitis. Most of the cases of paralysis occurred
one to two weeks after the injection of the arsenic.
The foregoing reports indicate that poisons can cause polio-
myelitis. It would appear that not any one poison in particular
would be responsible for all cases of poliomyelitis but the effect
of any one of several could produce the same ultimate result. When
a disease is known to be caused by a poison, it is obvious that a
search for a germ or virus in relation to it would not be made.
Conversely, if a so-called virus is believed to be associated with
the disease, then the possibility of poisoning as the cause of the
disease would not be considered. It will be shown, moreover, that
some so-called virus diseases and virus inclusions can be caused
by poisons.
Dr. Robert W. Lovett** of the Massachusetts State Board of
Health (1908), describing the epidemic of poliomyelitis in Massa-
chusetts in 1907, and after reviewing the medical literature on
experimental poliomyelitis, states: “The injection experiments
prove that certain metallic poisons, bacteria and toxins have a
selective action on the motor cells of the anterior cornua when
present in the general circulation; that the paralysis of this type
may be largely unilateral ; that the posterior limbs are always more
affected than the anterior ; and that the lesions in the cord in such
cases do not differ from those in anterior poliomyelitis.” It ap-
pears to be of great importance that the various poisons, lead,
arsenic, mercury, cyanide, etc., found capable of causing paralysis
are employed in relation to articles of food that are used for human
consumption.
There are two abnormal findings in cases of poliomyelitis that
point strongly to poisoning as the cause of this disease. One con-
sists in the appearance of increased amounts of porphyrin in the
urine® ; the other is the presence of increased amounts of guanidine
in the blood. It is a well-known fact that porphyria can follow
poisoning by a number of chemicals. Guanidine® * has been found
in increased amounts in the blood in arsenic, chloroform, and
carbon tetrachloride poisonings.
The fact that ascorbic acid has been effective in the treatment
of poliomyelitis* appears justly to imply that this disease has a
poison cause. Ascorbic acid has been used as a reducing agent
in the treatment of poisoning resulting from a number of toxic
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agents, including coal tar antipyretics, nitro compounds, analine,
cyanide, benzene, lead, arsenic, etc.**** Paralleling these modern
scientific investigations is the observation over a century ago that
lime juice and lemon juice were protective against the poisoning
by fish which sometimes resulted in paralysis.” This early ob-
servation is perhaps the principle reason why lemon juice is cus-
tomarily served today when fish are eaten.
The fact that methylene blue,“ another reducing agent, is effec-
tive in the treatment of poliomyelitis also points to the poison
cause of this disease. Methylene blue has been used as an anti-
dote in the treatment of nitrite, cyanide, carbon monoxide and
other poisonings.
Another fact that strongly implies that human poliomyelitis is
caused by a poison is found in the recent report (1951) by Dr.
Irwin S. Eskwith* of Bridgeport, Conn., that BAL (dimercaprol )
was effective in bringing about complete recovery in a moribund
4¥,-year-old girl with bulbar poliomyelitis. BAL counteracts the
effects of poisons; it has been shown not to be effective in infec-
tious diseases.
RELATIONSHIP OF HARVEST TO POLIOMYELITIS
It is a well-known fact that certain plants have natural poisonous
properties, for example, toadstools, but it is not generally realized
that some natural foods that are usually considered to be whole-
some and nutritious may at times be poisonous. Such factors as
drought, or excessive rainfall, fertilization with nitrates, and the
character of the soil may result in the development of poisons in
plants that are ordinarily edible. The frequent observation that
epidemics of poliomyelitis often occur and not infrequently are
confined to districts affected by drought is noteworthy in this
connection.
The finger of suspicion has for centuries been pointed toward
food as the cause of paralytic affections occurring during the sea-
son when poliomyelitis epidemics are known to occur.
Creighton® (1891), writing on epidemics in Britain, stated that
in 1383, and before that there is unmistakable reference to many
fatalities, as well as serious maladies caused by eating damaged
fruit.
In the 16th Century epidemics in which no symptom or sign
of polioencephalitis, poliomyelitis, or cerebrospinal meningitis was
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Scosey: Poison Cause of Poliomyelitis 177
lacking, ergot, bad bread, sour apples, mushrooms and the like
were mentioned as causes.“
Cholera morbus, a disease which was known to physicians in
the past and in some respects resembles the poliomyelitis of the
present, was first described by Sydenham® in 1669. The cause
of this disease was attributed by medical writers since the time of
Sydenham to unripe fruits and vegetables, fish, shellfish, water,
miasm, etc. Cruvelier® (1833), as well as others, pointed out that
the patient presented the symptoms of poisoning, a fact which he
says was noted by Morgagni, and almost every writer since his
time.
Benjamin Rush® (1799), in describing summer and autumnal
fevers, points out the effects of drought on leaves, vegetables and
fruits, denoting the inferior size and quality of the latter. He
observed illnesses among birds and beasts and pointed out that
the brain was not infrequently affected in children. He advised
against the use of unripe and decayed fruits at such times.
The failure of the principle food crop—the potato—in Ireland,
in 1817 and 1849, * caused the people to eat new potatoes dug
soon after the seed was planted as we'll as weeds and _ shellfish.
Food was eaten raw or improperly cooked because of lack of fuel.
Epidemic fever, among other names, was the designation for the
illnesses that resulted. Paralytic manifestations were not infre-
quently observed as sequelae. Contemporary physicians noted that
the effect in some cases resembled that of a concentrated poison.
Harris® (1920) pointed out that potato poisoning from new
and sprouting potatoes can result in vomiting, diarrhea, colicky
pains, headache, slight fever and prostration. Partial paralysis may
at times occur. Colton™ (1917) described an epidemic of polio-
myelitis which he ascribed to the eating of potatoes that had been
affected by drought.
In 1907, Dr. H. C. Emerson,* Massachusetts State Inspector of
Health, District 14, investigating an epidemic of poliomyelitis in
that state, made a careful inquiry regarding the diet. No infant
who was fed exclusively on the breast developed poliomyelitis. He
found in six cases that fruit and berries had been a large item
of the diet. In the cases of two infants, bananas and berries had
been given in the diet in addition to breast milk. In three cases
of poliomyelitis, the illness was attributed to the eating of large
amounts of blackberries and blueberries. In one case the illness
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178 Scorey: Poison Cause of Poliomyelitis
was credited to eating heartily of English mulberries. In 39 in-
stances it was stated that food supplies were bought from fruit
and vegetable peddlers in their localities.
Milk, which at times is known to contain toxins resulting from
poisonous plants eaten by cows, especially when overgrazing be-
cause of drought, can cause illness in humans. Dingman® (1916)
reported a milk-borne epidemic of poliomyelitis and several similar
outbreaks have been reported since then that were traceable to
milk. Dr. Marsh Pitzman™ (1928) insisted that poliomyelitis is
caused by poisonous alkaloids eaten by cows, the poison being
conveyed to humans through milk. Louis Bromfield,” in his book,
“Out of the Earth,” endorses this explanation of poliomyelitis.
Chapman,” raised the question of food poisoning to explain the
epidemic of poliomyelitis in England in 1947, when he stated: “Is
it not possible that the present prevalence of infantile paralysis
may, in part at any rate, be due to some article in our restricted
and modified dietary? In the Central Provinces of India there
were after famine years widespread outbreaks of a form of spastic
paralysis, caused by the consumption of the millet, Lathyrus sativa.
In ordinary times this was used only as an adjunct to the other
grains, and it was only when used as a staple diet that the par-
alysis occurred. Is it not possible that in the modification of the
austerity diet we may have introduced some article which may be
causing this widespread epidemic?”
Toomey and August® (1932) pointed out that some authors
thought that poliomyelitis is a disease of gastrointestinal origin
which might follow the ingestion of foodstuffs. In 1933, they
noted that the epidemic peak of poliomyelitis corresponds with
the harvest peak of perishable fruits and vegetables. They called
attention to the fact that the disease occurs only in those coun-
tries which raise the same type of agricultural products. Dr. C. W.
Burhans,” one of the colleagues of the authors, thought that green
apples might be a factor in the etiology of poliomyelitis. Toomey
et al.*' (1943) point out that there is frequently a history of dietary
indiscretions previous to an attack of poliomyelitis. They suspected
that a virus could be found on or in unwashed fruit or in well
water during epidemics of poliomyelitis. Every year for eight
years, therefore, grapes, apples, peaches, and pears were collected
from the vineyards and trees in Northern Ohio at the time of the
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ripening. In none of their studies was the so-called virus of polio-
myelitis demonstrated when the washings of the fruit or the well
water were injected into experimental animals. However, no chem-
ical tests were made to determine whether or not a chemical sub-
stance on or within the fruit or in the well water, acting by oral
ingestion to produce poliomyelitis, was present.
Draper® (1935) recorded a series of cases of poliomyelitis which
he postulated originated from a Greek fruiterer. All of the cases
were in contact with the Greek as business associates, relatives or
customers, and there was nothing in the evidence to point to in-
fection being carried by the Greek himself other than the fruit
he supplied.
Leavell® (1936) suggested that the ingestion of uncooked fruits
and vegetables might be responsible for poliomyelitis.
Barber®™ (1939) reported four cases of poliomyelitis that devel-
oped simultaneously on the same day from the eating of straw-
berries in a single house of a boarding school. He says that the
simultaneous onset of these cases resembled food poisoning. The
seasonal and climatic incidence of poliomyelitis, he points out,
agree closely with the seasonal increase in the consumption of
fresh garden production, He says that the epidemiological distri-
bution of poliomyelitis resembles food poisoning.
Chenault® (1941) noted that the history of poliomyelitis points
to a “suggested parallelism between a number of epidemics and the
appearance of fresh fruits and vegetables.”
Goldstein et al. (1946) reported an epidemic of polioenceph-
alitis at a naval training school among the cadets. The epidemic
was explosive in character and involved over 100 persons. Epi-
demiological evidence suggested that some food served in the mess
hall was the cause of the disease.
Kovar* (1945) noted the frequency of acute gastrointestinal
upsets at the time of epidemics of poliomyelitis in Nebraska in the
years when severe drought and economic depression were preva-
lent. The symptoms and signs of many of his cases were similar
to those of preparalytic poliomyelitis, but the patients had negative
spinal fluids and recovered without paralysis. One case, a boy
aged 13 years, had a diet for a few days prior to his illness which
consisted of foods of harvest that are capable of producing gastro-
intestinal upsets. In another case, a boy 9 years of age, had eaten a
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180 Scosey: Poison Cause of Poliomyelitis
number of apples along with other fresh harvest foods the day
before the onset of his illness. A third child, age 15 years, had
been drinking large quantities of water and had had a very unbal-
anced diet for a week prior to his illness. Kovar considered the
symptoms in these cases that he had observed as gastrointestinal
in origin because the diets in each of his cases consisted in foods
capable in themselves of producing gastrointestinal upsets. He
says: “Because of the economic depression, proper food could not
be purchased, and because of the drought proper food could not
be obtained or raised.”
Gebhardt and McKay® (1946) found during an epidemic of
poliomyelitis in Utah that of a total of 206 patients surveyed, 192
persons, or 93.2 per cent, had one to two weeks prior to the onset
of the disease eaten fresh fruits. The authors found in Utah, New
York and California, during 1943, that the cases of poliomyelitis
paralleled the harvest peaks. Most of the multiple cases in families
were found to have developed at the same time, suggesting means
other than contact as the mode of spread. Among the fruits more
commonly eaten were apples, peaches and pears; tomatoes headed
the list of vegetables. The authors stated that the data appeared
to fit into the jigsaw puzzle of epidemic poliomyelitis.
Scobey®” (1946) in an article entitled, “Food Poisoning as the
Etiological Factor in Poliomyelitis” pointed out that the frequent
reports of poliomyelitis following the ingestion of mushrooms,
fruits, vegetables, and milk could be attributed to the cyanide con-
tent of these foodstuffs. In a later report,”® he pointed out that
water, under certain conditions, especially drought, could also con-
tain cyanide.
It is well-known to veterinarians and farmers that certain grasses,
including Johnson grass, Sudan grass, millet, etc., affected by
drought, fertilization by nitrates, and other factors, contain a
high percentage of cyanophore glucosides capable of producing
hydrocyanic acid resulting in paralysis and death by respiratory
paralysis of cattle. Leaflet 88, U. S. Department of Agriculture,
entitled, “Poisoning of Livestock by Plants that Produce Hydro-
cyanic Acid” describes the effects of these plants on cattle. Cyanide
is found also in plants that belong to the rose family, which in-
cludes many of our common fruits, and in members of the mustard
family, including cabbage, etc. It has been demonstrated that mem-
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bers of the mustard family have goitrogenic properties in addition
to the effects that have been mentioned.
Abbott" (1948), of Auckland, New Zealand, stated: “The pub-
lic has always been fully convinced that they caught poliomyelitis
from one another by direct infection. The ‘germ’ idea is indeed
deeply ingrained in both the profession and the public. It will be
many years before our prolific writers of medical textbooks attain
the degree of sophistication that would enable them to understand
how and why poliomyelitis would be much more likely to be con-
tacted from the flour-bag, or some other homely article of food,
rather than from their neighbors.”
Adamson et al." (1949) reported an epidemic of poliomyelitis
in the Arctic involving 78 Eskimos between the ages of 8 and 64
years. The explosive and devastating character of the epidemic
strongly suggests food poisoning as the etiological factor. This
conclusion is borne out by noting that there had been a scarcity
of food and there was gouging of food when a supply was obtain-
able; the Eskimos had little regard for the state of preservation
of the food and showed marked preference for meat when it was
“high”; the eating habits were irregular, with a minimum amount
of preparation and cooking; not a child under three years of age
was afflicted with the disease since Eskimo mothers nurse their
babies until that age; gastrointestinal disorders were noted to be
more prevalent than usual during epidemics of poliomyelitis.
Barondes™ (1949) points out that a study of the epidemiology
of poliomyelitis shows a definite correlation with the harvesting
of fruit and vegetable crops and to changes in climate, weather
and humidity. The harvesting of such fruits as cherries, grapes,
berries, apricots, etc. and the edible vegetables, as lettuce, radish,
cucumbers, etc. usually from June to September, corresponds with
the period of poliomyelitis epidemics, Barondes points out.
Toomey et al.* (1949) made some important experimental ob-
servations that appear to show a correlation of the poison and
virus theories of poliomyelitis. They considered it possible that a
food (fruit) which enters the gastrointestinal tract could in some
way act as a precursor or catalytic enzyme on a normal constituent
of the tract and accelerate the production of poliomyelitis. Various
materials, together with fruit extracts, were tested.
When supernates of peach skin mash were injected intracere-
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brally into cotton rats, followed at intervals with intracerebral in-
jections of the so-called poliomyelitis virus, accelerated production
of paralysis occurred. Because of the presence of cyanophore gluco-
sides in peach skins, a synthetic preparation, succinonitrile, was
injected intracerebrally into the experimental animals. This chemi-
cal accelerated the production of the disease similar to that pro-
duced with the peach supernates. Toomey et al. emphasize that
the injections of fruit supernates were made in a manner that does
not occur under natural circumstances.
Sabin® (1951), although insisting on the virus etiology of polio-
myelitis, implicates food and drink as important factors in the
cause of this disease. He points out that measures which are
often advocated to combat poliomyelitis epidemics are not war-
ranted, such as (a) avoidance of crowds, large gatherings or
sports events, (b) exclusion of children under 16 years of age
from movies, churches, or schools, and (c) exclusion of polio-
myelitis patients and suspects from general hospital wards.
The material presented above appears clearly to indicate that
there is a correlation between the harvesting of fruits and vege-
tables and epidemics of poliomyelitis. Epidemics of this disease
usually appear in June and reach their peak in August and Sep-
tember. They usually terminate with the first frost which kills
vegetation. They are intensified in years of drought and are more
prevalent in drought affected areas. The majority of poliomyelitis
cases occur in rural areas and villages rather than in large cities.
The foregoing material shows also that when careful inquiries are
made concerning the diets of poliomyelitis patients prior to the
onset of their illnesses, valuable information is obtained. Dietary
histories, unfortunately, are rarely obtained from poliomyelitis
patients because it is generally assumed that a virus derived from
an active case or carrier is the cause of the disease. The implica-
tions should be obvious that investigation of foods eaten by the
poliomyelitis victim prior to his or her illness should be carefully
considered.
THE PRODUCTION OF SO-CALLED VIRUS DISEASES AND “VIRUS”
INCLUSIONS BY POISONS
The public, as well as many physicians, is under the impression
that viruses are living organisms comparable to a germ that en-
ters the human, animal or plant to cause the disease. The scientists,
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who are authorities on virus diseases, are in disagreement as to
the nature of a virus.
It is not generally realized that some so-called virus diseases
may result from the effects of poisons on the human body. Thus,
herpes zoster may follow exposure to carbon monoxide or the
administration of arsenic, bismuth, lipiodol, gold, mercury, tuber-
culin, alcohol, etc. An epidemic of herpes zoster and peripheral
neuritis, similar to the “jake” paralysis epidemic in this country,
followed the ingestion of arsenic in beer in Manchester, England
in 1900.**"* The toxic agent was determined to be arsenic arising
from dextrose made from starch by the use of crude sulfuric acid
containing this poisonous substance.
Herpes simplex, another so-called virus disease, has followed
the ingestion of alcohol, benzol, arsenobenzol, mercury, and the
inhalation of ether, among other poisons. Van Rooyen” noted its
appearance after sulfapyridine therapy. Herpes simplex has fol-
lowed the injection of vaccines, milk and colloidal metals.
Inclusion bodies have been defined as products of virus activity
or the elementary virus bodies themselves. Inclusion bodies have
been found in poisoned humans and experimental animals.
Dalldorf and Williams® (1945) found large acidophilic inclusion
bodies in the kidneys of rats poisoned by lead. Blackman* (1936)
found intranuclear inclusion bodies in the tubular epithelium of the
kidney and in the liver cells of 21 children dying from the effects
of acute lead poisoning and lead encephalitis.
Cox and Olitsky® (1934) found that the injection into animals
of aluminum hydroxide produced inclusion bodies similar to those
seen in infectious encephalitis.
Van Rooyen and Rhodes,® in their textbook (1948), “Virus
Diseases in Man,” state: “Histological changes similar to those
seen in infectious encephalitis may be produced by carbon mon-
oxide poisoning, brain injury, arteriosclerosis, uremia, pregnancy
toxemia and toxic agents like alcohol and lead.”
Olitsky and Harford®* (1937) were able to produce inclusion
bodies indistinguishable from those observed in virus infections
by the injections of aluminum compounds, ferric hydroxide and
carbon.
MISTAKES THAT HAVE BEEN MADE IN THE PAST
Several commissions, appointed during the first quarter of this
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century to investigate the cause of pellagra, concluded from their
studies that pellagra was an infectious, contagious disease. Harris*®
(1913) was able to inject Berkefeld filtered tissue material from
pellagra victims into monkeys to cause a corresponding disease
in these experimental animals. He concluded from these experi-
ments that a virus was present in the injected material and that
it was the cause of pellagra. If the work of Harris had been
followed exclusively, various strains of this “virus” might have
been discovered and a vaccine, effective in experimental animals,
might have been developed, as in the case of poliomyelitis. Today,
as a result of unlimited research, however, we know conclusively
that pellagra is not caused by a virus but rather that it is a vitamin
deficiency disease. It is obvious that if the investigations of pel-
lagra had been restricted to the virus theory, it would still be a
mystery.
Years ago, the disease known as milksickness in humans and
trembles in cattle was classified in medical textbooks as an infec-
tious disease. Stevens*® (1922) classified milksickness as a disease
caused by a filterable virus in his textbook “The Practice of Medi-
cine.” This disease was fatal to Nancy Hanks, mother of Abraham
Lincoln.
Milksickness appeared in epidemics, similar to poliomyelitis,
beginning in June and terminating with the first frost. The disease
had an incubation period similar to infectious diseases; there was
often a history of exposure to other cases of the disease; and it
had the power of self propagation similar to virus infections. It
was well-known, as in the case of poliomyelitis, that chilling and
fatigue would precipitate an attack of the disease. Like poliomye-
litis, milksickness occurred more frequently in rural districts than
in cities,
Farmers had suspected for many years that milksickness and
trembles were caused by a poisonous plant eaten by cattle. In fact,
Dr. Daniel Drake, a general practitioner (1810), published an
article entitled, “An Account of the Diseased State produced by
taking into the Stomach the Milk or Flesh of Cows which has
acquired deleterious properties from a vegetable sometimes eaten
by these Animals.”” However, the insistence by bacteriologists in
later years, who were able to influence the thinking of well-known
clinicians, that these diseases were caused by a germ or virus pre-
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cluded for some time serious consideration of the poison cause of
these diseases.
About 30 years ago, it was shown conclusively that milksickness
in man and trembles in cattle are caused by the poison tremetol,
an oily alcohol. This poison occurs in white snakeroot and rayless
goldenrod. When these plants are eaten by cattle, the poison is
conveyed to humans through the milk, milk products or the flesh
of the animals. Water borne epidemics have been reported which
resulted from the poisoning of the water by these plants.
The discovery of tremetol as the cause of these diseases ex-
plained why epidemics began in June and terminated with the
first frost* ; why chilling and fatigue** were factors in precipitating
an attack ; and why they appeared to be contagious. Huffman and
Couch (1942) state regarding these diseases: “The cause of the
disease was obscure and a great variety of guesses were current
among both laymen and the medical profession. . . . The isolation
of tremetol and the production of trembles by feeding poisonous
butter to sheep completed the chain of evidence linking the plants
to human milksickness and solved a mystery which for over 150
years had baffled physicians and terrorized dwellers in the rural
districts.”
The symptoms of milksickness in man resemble those of in-
fluenza or grippe, gastritis, and so-called ptomaine poisoning. As a
matter of fact, so-called summer grippe or flu often occurs during
epidemics of poliomyelitis. There were 10,000 cases in Cincinnati
in 1947,** * which were thought to be related to poliomyelitis and
were considered, therefore, virus infections. However, Matson”
(1950), writing about poisonous plants, says that some physicians
have expressed the opinion that mysterious outbreaks of so-called
summer flu in the late summer are often due to milk contaminated
with tremetol.
The observation that human and bovine outbreaks of tremetol
poisoning occur simultaneously corresponds with similar observa-
*Although epidemics of milksickness and trembles usually occurred during the growth
period of the poisonous plants, they appeared occasionally even during the winter because
of the presence of the poison in stored hay, beef, pork, butter, cheese, honey, etc.
**It was the custom of people in affected districts to chase their beef cattle around
with dogs until they were heated by the exercise; then if the cattle did not show any
signs of the disease they were killed and eaten as beef without fear. Dixon® (1833)
states concerning milksickness in man: “It is one of the peculiarities of the disease that
the poison occasionally lies long dormant in the system, and only becomes active by
some indiscretion or violent bodily exertion.”
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186 Sconey: Poison Cause of Poliomyelitis
tions made during epidemics of poliomyelitis. Medical reports have
shown repeatedly that paralytic diseases in horses, pigs, dogs, cats,
ducks, chickens, etc. occur simultaneously in districts where epi-
demics of poliomyelitis are prevalent.
FACTORS PRECLUDING INVESTIGATION OF THE POISON CAUSE
OF POLIOMYELITIS
It is obvious that in the study of poliomyelitis every possible
cause, including the possibility of poisoning, should be investi-
gated.
Since 1908—for 44 years—poliomyelitis research has been pre-
dominantly directed along only one line of investigation, i.e., the
infectious theory. This single line of study, precluding other possi-
bilities, including the poison cause of the disease, has resulted from
two factors, (1) The Public Health Law,” and (2) the insistence,
based entirely on animal experiments, that poliomyelitis is caused
by a virus.
1. The Public Health Law. The inclusion of poliomyelitis in
the Public Health Law as a communicable, infectious disease dates
back to the early part of the 20th Century. At that time many
diseases, now known to be neither communicable nor infectious,
were considered to be caused by an infectious agent simply because
they occurred in epidemics. The general attitude of that period
is expressed by Sachs” (1911) in his statement: “In general, the
epidemic occurrence of any disease is sufficient to prove its infec-
tious or contagious character.” The vitamin deficiency diseases,
beriberi and pellagra, are outstanding examples of epidemic diseases
that were formerly considered to be infectious and communicable
according to the logic employed by Sachs. In fact, we find pel-
lagra incorporated into the Public Health Law as a communicable
disease in the State of Pennsylvania in the following rule and regu-
lation adopted January 5, 1910: “That all physicians practicing
within the limits of the state shall make immediate report of each
and every case of uncinariasis duodenalis (hookworm disease)
and pellagra and anterior poliomyelitis (infantile paralysis) occur-
ring in their practice in the same manner that other communicable
diseases are now by law and by rule and regulation of the State
Department of Health reported to the health authorities.” A State
Health Officer’® recently wrote to me as follows: “I think all of
us will agree with you that in the past, as is still probably true,
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public health rules and regulations and sometimes even public
health laws, were influenced too much by what we did not know
rather than by what we did know. This was probably an acceptable
line of reasoning in the past, but with increasing public health
education and greater understanding and cooperation from citi-
zens, this justification becomes less acceptable.”
The fact that an extensive epidemic of poliomyelitis was prevail-
ing in the states of New York and Massachusetts in 1907, aroused
the suspicion that the disease was infectious and communicable ;
it was therefore incorporated into the Public Health Law as such.
However, conclusive evidence of contagiousness was not estab-
lished during that epidemic nor in subsequent ones. Moreover,
conclusive evidence of contagiousness was not established in 1949,
during the greatest epidemic of poliomyelitis in recorded history,
as shown by the records of the U. S. Public Health Service and
the New York State Department of Health. Time Magazine,”
commenting on these surveys, points out how, when and where
people catch polio remained a mystery. In addition to the failure
to prove contagiousness of human poliomyelitis, it has likewise
been impossible to prove contagiousness of poliomyelitis in experi-
mental animals. This fact will be considered in detail later.
As a result of the inclusion of poliomyelitis in the Public Health
Law as a contagious, communicable or infectious disease, investi-
gations regarding it are almost exclusively in the hands of special-
ists in virology and public health. The country doctor, general
practitioner, and clinician have little or no opportunity to partici-
pate in poliomyelitis research under these circumstances. Yet, Dr.
W. Ritchie Russell” of the Department of Neurology, United
Oxford Hospitals, Oxford, England stated in 1950: “Clinical
research into this disease is so much neglected that there are
exciting discoveries waiting for anyone with time to give to this
type of investigation.”
Medical advances of the utmost importance have been made
in the past by general practitioners. An outstanding example is
the work of Dr. Edward Jenner, a general practitioner in Glouces-
tershire, England, whose observations and deductions brought
about vaccination against smallpox. All advances in medicine
do not result from laboratory experiments. Any doctor in any
community, however small, and however limited his opportunities,
may make a fundamental discovery, but he must be given the
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opportunity to participate in the program and his observations
and deductions must be given adequate consideration.
2. Virus Research. The more or less general acceptance of the
idea that poliomyelitis is caused by a virus arose from experimental
animal studies by Landsteiner*’ (1908) in Austria, and Flexner
and Lewis” (1909) in the United States. These experiments
showed that a substance obtained from poliomyelitis victims could
produce a paralytic disease when administered to experimental
animals. It has been assumed, as a result of these experiments
that an exogenous virus is the cause of human poliomyelitis. Dr.
Harold L. Amoss’ stated in 1928: “By reason of the parallelism
of the human and experimental disease it is believed that inferences
drawn from experiments with monkeys may be accepted with a
certain degree of safety as applicable to the solution of problems
in connection with human cases.” The portal of entry of the so-
called virus of poliomyelitis into the human body never has been
established. The question of the portal of entry is summed up
in the published reports of the International Poliomyelitis Con-
gress’ that was held in New York City in 19448. The Modulator
stated: ‘“‘We do not know too much about the portal of entry in
human beings,”’ and Dr. John R. Paul, of Yale University, stated :
“IT would say we do not know the portal of entry in human beings.”
It was mentioned in the foregoing that human poliomyelitis has
not been shown conclusively to be a contagious disease. Neither
has the experimental animal disease, produced by the so-called
poliomyelitis virus, been shown to be communicable. Rosenau™
(1921) stated : “Monkeys have so far never been known to contract
the disease ‘spontaneously’ even though they are kept in intimate
association with infected monkeys.” Twenty years later (1941),
Dr. John A. Toomey,’ a poliomyelitis authority, stated: “No
animal gets the disease from another no matter how intimately
exposed.”
It is extremely difficult to understand how a human can contract
poliomyelitis from another individual through dissemination of a
virus by contact, carriers, excrement, unclean hands, unwashed
fruits and vegetables, flies, etc. when a healthy animal in the same
cage with an “infected” animal, exposed to all of these natural
factors, remains unaffected. It appears obvious, therefore, that
communicability should have been established conclusively both in
humans and in experimental animals before poliomyelitis was in-
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corporated into the Public Health Law as a communicable disease.
Some investigators have as a matter of fact pointed out that
human poliomyelitis and the disease produced in experimental
animals from human material, etc. are not the same disease.
Toomey™ (1935), for example, stated that intranasal and intra-
cerebral inoculation of poliomyelitis virus in the monkey does not
produce the same disease that is seen in man. Dr. Claus W.
Jungeblut,’” a well-known bacteriologist who has worked on the
poliomyelitis problem for many years, recently stated (1950):
“Whatever the final answer may be, it seems a reasonable state-
ment at this time that the highly specialized, neurotropically fixed
virus, which has been maintained in the past by intracerebral
passage in rhesus monkeys, is more likely a laboratory artefact than
the agent which causes the natural disease in man.” The logical
conclusion appears to be, therefore, that the laboratory experiments
with the so-called virus of poliomyelitis are merely of academic
interest and have no practical application to human poliomyelitis.
Jelliffe,"°* 32 years ago, cautioned: “The purity of laboratory
experiments is rarely repeated in nature.”
For almost half a century poliomyelitis investigations have been
directed towards a supposed exogenous virus that enters the
human body to cause the disease. The manner in which the Public
Health Law is now stated imposes only this type of investigation.
No intensive studies have been made, on the other hand, to deter-
mine whether or not the so-called virus of poliomyelitis is an
autochthonous chemical substance that does not enter the human
body at all, but simply results from an exogenous factor or factors,
for example, a food poison. Analogous reactions are well-known
as illustrated by the production of experimental sarcomas by indol,
arsenic, tar, etc. and which have been transmitted by Berkefeld
filtrates.
The discovery in recent years of the so-called Coxsackie virus
has tended to further confuse the entire poliomyelitis problem.
Hoyne™ (1951), for example, states that the announcement of this
discovery “is accompanied by some feeling of dismay. .. . In view
of the foregoing announcement it seems that trained investigators
have added one more problem to the nebulous conditions enveloping
poliomyelitis. One might also be tempted to make the statement
that the more we learn about poliomyelitis, the less we know.”
Hoyne’s statement applies obviously to the confusion that has arisen
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from exclusive virus studies in poliomyelitis. A Lancet editorial’
(1951) also indicates the complexity of the problem brought about
by the discovery of the Coxsackie virus, as follows: “A crop of
new snags is coming along as every week brings new tidings of
the Coxsackie viruses.”
Many diseases have been considered to be caused by viruses but
virus studies constitute only a portion of the investigations intended
to determine the cause of the disease. Poliomyelitis investigations,
on the other hand, have been confined exclusively to virus studies.
) Because of this situation and the Public Health Law, those who
maintain other opinions, including those concerning poisons as the
cause of poliomyelitis, can neither obtain funds from any source
for research nor cooperation for investigating their ideas. Reap-
praisal and investigation of all theories, infectious and non-infec-
tious, are imperative.
To epitomize, the following quotation from a talk on poliomyelitis
: given by Dr. Ritchie Russell,” Department of Neurology, United
Oxford Hospitals, Oxford, England (1950) summarizes what has
been pointed out in the foregoing: “The time is ripe for a survey
: of our knowledge of the disease, of the methods of treatment we
‘ are accustomed to use and our efforts to advance knowledge of
/ the condition. . . . Surely if the Americans with all their millions
of dollars for research on poliomyelitis can do so little, we need
not try... . 1 do not intend here to praise good work that has
been done, but more to emphasize the gaps in our knowledge of
the disease in the hope that others may be encouraged to work
on the subject which sorely needs some extra attention. There
are at present several different groups of specialists working on
. the disease, including virologists, infectious disease physicians,
orthopedic surgeons, physiotherapists and public health officers.
This may be a reasonably adequate state of affairs as far as handling
the individual case is concerned ; but as a background for advanc-
ing knowledge of the disease it is not satisfactory for the members
of each of these groups have many other interests, and have neither
the time nor always the experience of other aspects of the disease to
enable them to fit their piece into the whole picture in such a way
as to advance research. . . . Unfortunately, the disease gets worse
as public health improves, and measures which are designed simply
to avoid infection seem to be singularly ineffective in poliomyelitis.”
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This statement is reminiscent of one made in 1938 by Dr. Carl C.
Dauer,'” Chief of the Bureau of Preventable Diseases, District of
Columbia Health Department, viz: “It seems rather remarkable
in spite of all the time and effort spent in poliomyelitis studies
during the past 20 years so little information in the epidemiolog °
of the disease has been produced.”
The urgent need for cooperation between the clinician and labor -
atory worker, as well as an unprejudiced attitude toward the
poliomyelitis problem, is emphasized by Jungeblut'® as follows:
“The subject is of keen interest to clinicians and laboratory workers
alike and progress will be measured by the extent of cooperation
between the two. Until the final word has been said it is hoped
that, in the future, students of poliomyelitis will preserve an
open mind and maintain an open door in their efforts to unravel
the mysteries of this baffling disease.” Jungeblut indicates the
confusion that has been caused by the virus theory when he states:
“Actually, the history of this disease has been marked by periods
of violent disagreement among scientific workers and by sharp
dissension within the ranks of the medical profession.”
SUMMARY
1. The poison cause of paralysis has been known for many
years, Poliomyelitis, resulting from poisons, has been demonstrated
clinically in humans and produced artificially in experimental
animals,
2. A relationship between harvest and poliomyelitis has been
suggested repeatedly. At such times, corresponding with epidemics
of poliomyelitis, some foods of harvest may be poisonous as a
result of fertilizers, insect sprays and intrinsic chemical changes.
3. Some so-called virus diseases and virus inclusions may result
from poisons.
4. Mistakes have been made in the past whereby diseases con-
sidered to be infectious and communicable were later conclusively
shown to be neither infectious nor communicable but related to
vitamin deficiency or food poisoning.
5. The investigation of the poison cause of poliomyelitis has
been obstructed by the Public Health Law which has made this
disease legally communicable and infectious. This legal acceptance
of the infectious origin of poliomyelitis is, moreover, in a large
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degree responsible for exclusive virus studies in determining the
cause of this disease.
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Linn, C.: Frumusan, P. and nll R: Bull, et mém. Soc. méd. d. hép. de
Paris, 55: 1194-1203, July 17, 1939.
Carmick, M.: Polis, B. D. and Klein, T.: Arch. Int. Med., 78: 296-302, Sept.
. J.: Gilchrist, M. and White, J. C.: Biochem. J., 38: 8, 1944.
>. S.: J. Biochem., 143: 439-446, April 1942.
; , O. H.: Biochem, J., 37: 615-618, 1943.
Chisholm, C.: Edinburgh M. & S. J., 4: 393-422, Oct. —.
Burrows, G. M.: London Med. Repos., 3: 445-476, June 1, 1815.
Massi, L. and Postorini: Riv. di clin. pediat., 44: 196- 198, March 1948.
Eskwith, Irwin S.: Am. J. Dis. Child., 81: 684- 686, May 1951.
Creighton, Chasis History of Epidemics in Britain, 1891.
Crookshank, F. : Boston M. & S. J., 182: 34-35, "Jan, 8, 1920.
Sydenham, T.: The works of Thomas "Sydenham on Acute and Chronic Diseases
by George Wallis, Vol. 1, 1788.
Cruvelier, P. J.: ‘Abstr. Am. J. Med. Sc., : 442-456, 1833.
Rush, Benjamin: Medical Inquiries and aa on Vol. 4, 2nd. Ed., 1805.
Law, Robert: Dublin J. M. Sc., 15: 1-86, Aug. 1849.
Purefoy, T.: Dublin M. Sc., 16: 318-331, 1853.
Harris, S.: Food Poiscning: Tice’s Practice of Medicine, Vol. 8, 1928.
Colton, M. H.: Virginia M. Semi-Monthly, 22: 457, 1917.
Emerson, H. C.: Boston M. & S. J., 151: 115-119, July 22, 1909.
Dingman, J. C.: New York State in Med., 16: 589, 16
Pitzman, Marsh: J. Missouri M. A., 25: 249- 257, AL. 19, 1928.
Bromfield, Louis: Out of the Earth, PP, 43-45, 1950.
Chapman, Col. P. F.: Brit. M. J., 398, Sept. 6, 1947.
Toomey, J. A. and August. M. H.: 2 Pediat” 1: 601-607, Nov. 1932.
Toomey, J. A. and August, M. H.; Am. J. Dis. Child., 46: 262-279, Aug. 1933.
Toomey, J. A.; Tackacs, W. S. and Tischer, M. D.: J. Pediat., 23: 172, Aug.
1943.
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16.
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18.
24.
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26.
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30,
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32.
33.
34.
36.
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41. 4
43.
45.
46.
49.
50.
$1.
52.
53.
54
55.
56.
$7. a
58. 4
59.
60
61.
4
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Sconey: Poison Cause of Poliomyelitis
Draper, George: Infantile Paralysis, 1935.
Leavell, H. R.: Kentucky M. J., 34: 110, March 1936.
Barber, G. O.: Brit. _ | ae i137, Dec. 7, 1938.
Chenault, Z. W. J. M. A., 33: 220, x t. 1941.
Goldstein, Lt. Col. D 1H; Hammon, Ww. . and Vietes, H. R.: J. A. M. A.,
131: 569-573, June 15,
Kovar, W. R.: Nebraska a J., 30: 394, Oct. 1945.
. Gebhardt, L. P. and McKay, M. H.: y Pediat., 28: 1-13, Jan. 1946.
Scobey, R. R.: Arcu. Peptart., 63: 322-354, July 1946.
Scobey, R. R.: Arcu. Peptat., 63: 567- 580, Nov. 1946,
Abbott, W. N.: Poliomyelitis in Relation to the Recent Advances in Our Tech-
— and Concepts Concerning Protein, Radiation and Viruses (Monograph),
48.
Adamson, J. D.: Moody, J. P.; Peart, A. F. W.; Smillie, R. A.; Wilt, J. C
and Wood, W. J. L.: Canad. M. A. J., 61: 339-348, Oct. ~~.
Barondes, R. de Rohan: Mil. Surgeon, 105: 400-408, Nov.
a - A.: Takacs, W. S and Pirone, P. P.: Am. tt Dis. Child., 78: 1-15,
uly 1949.
5 , A. B.: J. Pediat., 39: 519-531, Nov. 1951.
Row, N.; Barent, F. H. and Warrington, W. B.: Brit. - J : 10, Jan. 5, 1901.
Reynolds, C. S. et - Brit. M. J., 2: 1044-1049, Oct. 12, 1
Editorial: Boston M. S. J., 150: 49-50, Jan. 14, 1904.
ae, Cc Rhodes! J. and Ewing, A. C.: Brit. M. J., 2: 28-301, Aug.
Datidod, G. and Williams, R. R.: Science, 102: 8-670, Dec. 28, 1945.
Blackman, S. S. Jr.: Bull. Johns Hopkins Hosp., 58: 384-404, 1936.
Cox, H. R. and Olitsky, P. K.: Science, 79: 459, 1934.
Van Rooyen, C. E. and Rhodes, A. J.: Virus ~ a ig Man, 1
Olitsky, P. K. and Harford, C. G.: Am. J. Path., 13: 729-747, Pa 1937.
Harris, W. M.: J.A.M.A. @: 1948-1950, June 21, rH
Stevens, A. A.: The Practice of Medicine, pp. 294-295, 1922.
Drake, Daniel: Quoted by Jordan, E. O. and Harris, N. M., J. Infect. Dis., 6
401-491, Sept. 2, 1909.
yore W. T. and Couch, J. F.: Plants Poisonous to Livestock, Yearbook of
p. 366, 1942
Fs A. B. and Steigman, A. d: Am, J. Hyg., 49: 176-193, March 1949.
Editorial: “Gaon Housekeeping Magazine, ». 30, Aug. 1949.
Matson, V. : Today's Health, BB: B, May 1950 9
ag uote by Jordon, E. O. and Harris, N. M.: J. Infect. Dis., 6: 401-491,
pt. 20,
Scobey, R. R.: Arcu. Pepiat., 68: 220-232, May 1951.
Sachs, B.: Am. J. Obst. & Gynec., 63: 703-710, April 1911.
Thompson, G. D. Carlyle, Executive Officer, State Board of Health, State of
Montana: Personal Communication
Editorial: Time Magazine, Jan. 2, 1950
Russell, W. Ritchie: J. Bone & Joint Surg., 32B: 748-750, 1950.
Landsteiner, K.: Wein. klin. Wchnschr., 1908.
Flexner, S ‘and Lewis, P. A.: J.A.M.A., 639, Nov. 13, _
Amoss, Harold L.: Tice Practice of Medicine Vol. 5, p. 335,
Published Reports: International Poliomyelitis Congress, P, wari 1948.
Rosenau, M. J.: Preventive Medicine and Hygiene, 4th Ed., p. 389, 1921.
Toomey, J. A.: J. Pediat., 19: 103, July 1941.
Toomey, J. A.: Science, 82: a», Aug. 30, 1935.
Jungeblut, Claus W.: J. Pediat., 37: 109-128, July 1950.
Jelliffe, S. E.: J. Nerv. & Ment. Dis., 49: 522, May 1919.
Hoyne, A. L.: Clin. North America, Number, 175-188, Jan. 1951.
Editorial: Lancet: 2: 1173-1174, Dec. 22, 1
Dauer, Carl C.: Pub. Health Rep., 53: 1005-1084, June 24, 1938.
1411 So. Salina St.
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DEPARTMENT OF ABSTRACTS
Rocers, H. M.: DisrurBANcES OF CARDIAC RHYTHM AND
CONDUCTION IN CONGENITAL CarpDIAc DISEASE: REPORT OF
Five Cases. (Annals of Internal Medicine, 35 :1276, Dec. 1951).
Complete heart block is probably the most commonly recorded
conduction disturbance observed in association with congenital
cardiac disease. This ectopic rhythm is most often observed in
association with congenital ventricular septal defects. Auricular
fibrillation has been observed to occur frequently in association with
defects of the atrial septum. This anomally may also be associated
with paroxysmal tachycardia, auricular flutter and comulete heart
block. A case was recently reported of paroxysmal tachycardia
with an atrial septal defect in which death was presumably the
result of the ectopic rhythm. The Wolff-Parkinson-White syn-
drome has been observed in association with coarctation of the
aorta. However, recorded arrhythmias and disturbances in cardiac
conduction in association with congenital cardiac disease are not
common, Micuae A, Brescia, M.D.
MANNING, M. I’. anp Yu, P. N. G.: ELecTROCARDIOGRAPHIC
CHANGES IN oLiomMyeLitis. ANALYsis or 150 Cases. (Amer-
ican Journal of the Medical Sciences, 222 :658, Dec. 1951).
Of 150 cases of acute poliomyelitis studied, 116 showed abnormal
electrocardiograms sometime during the disease. The most com-
mon findings were, in order of frequency, abnormal T waves,
tachycardia, and abnormal QT. The incidence of abnormal EKG
changes was higher in adults than in children, and in patients with
bulbar or high cervical paralysis than in those with other types of
lesions. Of 8 fatal cases autopsied, 2 showed evidence of myo-
carditis. Also noted in the fatal cases were pulmonary edema and
other complications and dilatation of the right ventricle. In the
majority of the patients the abnormal changes appeared and re-
verted to normal within the first 4 weeks. However, a small num-
ber of patients still showed abnormalities several months after the
onset of the disease. Micuae A. Brescia, M.D.
TAukA, H.: Tue Weicut or tHe THYMUS IN CHILDREN OF
0-2 Years or Ace. (Acta Paediatrica, 40:469, Nov. 1951).
194
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Department of Abstracts 195
The thymus of 309 children, 0-2 years of age, who died from
various diseases, has been weighed at autopsy. Age has no definite
influence on the weight and the individual’s variations are great, in
full term infants varying from 0.50 to 28.55 g. and in prematurely
born children from 0.20 to 12.93 g. During the last weeks of preg-
nancy the thymus seems to increase in size and the size is not
influenced by the sex of the infant. The size of the thymus is
influenced by the duration of the disease, decreasing rapidly with
the prolongation of the disease. It is also influenced by the nutri-
tional condition. Thus, the smallest thymuses were found in those
infants who died from chronic gastroenteritis. There were no
cases of the so-called “thymus-deaths.”
Micnuae A. Brescia, M.D.
(GUNNARSON, S. AND MELLIN, K. A.: THE ELECTROENCEPHALO-
GRAM IN Enuresis. (Acta Paediatrica, 40:496, Nov. 1951).
Ninety children with enuresis have been selected for an ence-
phalographic study. They have been divided into two groups, viz.,
those who have had a dry period for one year or more, and those
who have always been wet. There is, apparently, a marked differ-
ence between the EEG findings in these two groups, with a marked
preponderance of pathological records in the “never dry” group.
This supports the theory of immaturity in the nervous system as
the cause of enuresis in the always wet children. Attention is
drawn to the fact, that two epileptics occurred among these chil-
dren with enuresis. AutTHors’ SUMMARY.
Fisuer, B. M.; Roserts, G. AaNp HinsHuaw, H. C.: THe Sus-
CUTANEOUS ADMINISTRATION OF THE SopituM SALT oF PARA-
AMINOSALICYLIC ACID IN THE TREATMENT OF TUBERCULOSIS.
(American Review of Tuberculosis, 64:557, Nov. 1951).
The sodium salt of PAS may be given subcutaneously in solu-
tion of 1 to 2 per cent concentration in dosage of 6.25 to 39.5 gm.
per day (with hyaluronidase). The concentrations of PAS at-
tained in the blood are comparable to those noted after intravenous
administration of sodium PAS. Subcutaneous administration of
solium PAS is a safe, effective, well-tolerated method of PAS
administration and has the advantages of ease of administration
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196 Department of Abstracts
and applicability to infants, as well as permitting rest periods for
veins when parenteral PAS therapy is desired over extended pe-
riods. CBS fluid PAS concentrations of 14 mg. per 100 ml. have
been observed following the subcutaneous administration of 12.5 to
18.75 gm. of sodium PAS. Local reactions can be minimized by
slow administration of PAS solutions which do not exceed a 2
per cent concentration. Parenteral sodium PAS should be given
with caution to patients who have experienced systemic reactions
to PAS administered by the oral route and to patients with im-
paired renal function. AutTHor’s SUMMARY.
Cuitps, D. S. AND KENNEDY, R. L. J.: RetiIcuLo-ENpo-
THELIOSIS OF CHILDREN’S TREATMENT WITH ROENTGEN RAys.
(Radiology, 57 7655, Nov. 1951).
Twelve children with extensive reticulo-endotheliosis of the
Hand-Schuller-Christian type were treated with multiple low doses
of radiation. Three of the patients died of the disease : 9 recovered.
AuTHOR’s SUMMARY.
AveRBACH, O.: TUBERCULOUS MENINGITIS— CORRELATION OF
THERAPEUTIC RESULTS WITH THE PATHOGENESIS AND PATHOLO-
Gic CHANGES. IL. GENERAL CONSIDERATIONS AND PATHOGENESIS
(American Review of Tuberculosis, 64 :408, Oct. 1951). II. PatH-
oLoGic CHANGES IN UNTREATED AND TREATED Cases. (Ibid,
64 :419, Oct. 1951).
Tuberculous meningitis was present in 42.2 per cent of a series
of 97 fatal cases of tuberculosis in children and was usually re-
lated to a spread from a primary complex. The difference between
the pathogenesis of tuberculous meningitis may explain in part
the better results obtained in children than in adults who have
been treated with streptomycin. In children, the source of dis-
semination is eliminated by the healing of the primary infection,
whereas in adults the meningitis is generally secondary to an ac-
tive extrapulmonary tuberculosis which gives rise to repeated
hematogenous disseminations. Streptomycin prolongs the natural
course of tuberculous meningitis and also results in extensive heal-
ing changes within the exudate. The survival period in untreated
cases is generally less than three weeks, too early for extensive
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Department of Abstracts 197
caseation and granulation tissue. Under streptomycin therapy the
exudate within the subarachnoid space undergoes extensive necrosis
which encircles and partially involves the vessel walls. Con-
comitantly there is a fibrous thickening of the intima of the en-
closed blood vessels. Tuberculous granulation tissue which de-
velops from the pia arachnoid replaces the remaining fibroinocel-
lular exudate in the subarachnoid space so that, in cases receiving
prolonged therapy, the base of the brain is covered by a dense
layer of hyalinized connective tissue which encloses necrotic foci.
The course of the tuberculous meningitis in cases which receive
streptomycin therapy is similar to that in other serosal surfaces
in which the patients have survived the disease for long periods
of time. Micnwaec A. Brescia, M.D.
GREENBERG, M.; AprAmson, H.; Cooper, H. M. anp SoLomon,
H. E.: Tue Reration BETWEEN RECENT INJECTIONS AND
PARALYTIC POLIOMYELITIS IN CHILDREN. (American Journal of
Public Health, 42:142, Feb. 1952).
The inoculation histories of 1,300 children that had poliomyelitis
in New York City in 1949 and 1950 were analyzed. A relationship
was shown to exist between site of injection and site of paralysis in
children injected not more than a month before onset of poliomye-
litis with diphtheria toxoid, pertussis vaccine or tetanus toxoid,
or any combination of the three. This relationship was not clearly
shown to follow recent injections of penicillin or other agents. No
increase in bulbar cases or deaths resulted from previous injections.
The extra hazard of poliomyelitis as a result of recent inoculations
is small in children under 1 year of age and is negligible in infants
under 6 months of age. The authors suggest that routine immuni-
zations be suspended in older children during the poliomyelitis
season and in infants between 6 months to 1 year during epidemic
years. Infants under 6 months can receive immunizations at any
time. Therapeutic and immediate prophylactic injections should
not be discontinued at any time. | Micwaetr A. Brescra, M.D.
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BOOK REVIEWS
Rx For Mepicat Writinc. By Edwin P. Jordon, M.D. and
Willard C. Shepard. Cloth. Pp. 112. Illustrated. Philadelphia :
W. B. Saunders Co., 1952.
This is just the type of small volume that should be read before
attempting to write a medical article. It is as valuable to the neo-
phyte as to the veteran writer. It emphasizes the importance of
choosing the proper subject and writing carefully, reading and
revising several times to pick out and eliminate the clumsy sec-
tions of the article. The chapter on statistics touches on a deli-
cate problem. Practically everyone likes to use statistics, rightly
or wrongly. The authors show how to pick the proper statistics
and how to utilize them in writing or reading an article. There
are several appendices, including common abbreviations found in
medical manuscripts, proofreaders’ marks, equivalents of weights,
measures and dosages, and temperature conversion tables from
Fahrenheit to centigrade and vice versa.
Micuaet A. Brescia, M.D.
DyNAMic Psycuiatry (Basic Principles). By Louis S. London,
M.D. Cloth. Pp. 95. Price $2.00. New York: Corinthian Pub-
lications, Inc., 1952.
The first part of the text presents an evaluation of psychothera-
peutics. In reality, this section is an excellent history of mental
diseases from the primitive period through the 17th century. Libido
is defined and the theories relating to the libido of numerous
authors are considered. These include Freud, Jung, Abraham and
Searl among many others. The final chapter then discusses the
development of the libido in the child and its relation to various
complexes, such as oedipus, electra, etc. He finally concludes with
the development of the libido in the adult and its relation to the
neurosis, sexual deviations, manic-depressive psychosis, schizo-
phrenia and other psychoses. The text is well written, clear and
H. Frucuter, M.D.
concise.
198
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